Professional Documents
Culture Documents
Internal Medicine
Internal Medicine
+Causes Of Macroglossia :
.hypothyroidism
.down's syndrome
.acromegaly
.amyloidosis
**Dyspepsia
-Is term used to describe symptoms such as bloating and nausea which are thought to originate from the upper GI
-Dyspepsia is a common problem and is frequently caused by gastroesophageal reflux disease (GERD) or gastritis. It may be the
first symptom of peptic ulcer disease (an ulcer of the stomach or duodenum)
-Causes :
.psychological, anxiety, depression
.post infectious dyspepsia (is the term given when dyspepsia occurs after an acute gastroenteritis infection)
.systemic disease (renal failure, hypercalcemia)
.diseases of the gastrointestinal tract (GERD, peptic ulcer disease, gastritis, gastric cancer, esophageal cancer, coeliac disease,
food allergy, IBD, IBS, chronic intestinal ischemia, esophageal spasm, colonic carcinoma and gastroparesis)
.liver and pancreas diseases (cholelithiasis, gallstones, chronic pancreatitis, hepatitis and pancreatic cancer-metastasis)
.food or drug intolerance (overeating, eating too quickly, eating high-fat foods, eating during stressful situations, or drinking too
much alcohol or coffee)
2
-Diagnosis :
.people under 55yrs without alarm symptoms can be treated without investigation, but are considered for investigation for
peptic ulcer disease caused by Helicobacter pylori infection
.people over 55yrs with recent onset dyspepsia or those with alarm symptoms should be urgently investigated by upper
gastrointestinal endoscopy. This will rule out peptic ulcer disease, medication-related ulceration, malignancy and other rarer
causes
+Medication-related dyspepsia is usually related to NSAIDs and can be complicated by bleeding or ulceration with perforation
of stomach wall
-Treatment :
proton pump inhibitors (PPIs) - omeprazole (which are effective for the treatment of heartburn) (this drugs used to reduction of
gastric acid production)
**Dysphagia
-Is difficulty in swallowing
+Odynophagia (is painful swallowing, in the mouth or esophagus. It can occur with or without dysphagia)
-
Signs & Symptoms :
.swallowing difficulty
.difficulty controlling food in the mouth
.inability to control food or saliva in the mouth
.coughing
.choking
3
.frequent pneumonia
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-Investigation :
.endoscopy (investigation of choice)
.barium swallow (of abnormality is found in endoscopy)
-Treatment (treating dysphagia depends on the type and severity of a patient's swallowing difficulty) :
.for difficulties in the mouth and throat areas, treatments are generally focused on swallowing therapy, including exercises, and
dietary changes
.for problems in the esophagus, treatment options may include surgery or medicine
.feeding tubes are also options for treating dysphagia (nasogastric or endoscopic tubes)
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+The incidence of dysphagia is higher in the elderly, in patients who have had strokes, and in patients who are admitted to
acute care hospitals or chronic care facilities
**Achalasia
-Failure of relaxation of the lower oesophageal sphincter LES / Is a failure of smooth muscle fibers to relax, which can cause a
sphincter to remain closed and fail to open when needed
+Achalasia can happen at various points along the gastrointestinal tract; achalasia of the rectum, for instance, in Hirschsprung's
disease
-Characterized By :
.F > M / 40yrs of age
.regurgitation and aspiration pneumonia are common (food and liquid, including saliva, are retained in the esophagus and may
be inhaled into the lungs - aspiration)
.difficulty in swallowing (dysphagia - tends to become progressively worse over time and to involve both fluids and solids)
.regurgitation (of undigested food)
.sometimes chest pain (behind the sternum) (cardiospasm and non-cardiac chest pain can often be mistaken for a heart attack)
.weight loss
.coughing when lying in a horizontal position
+The M.C form is primary achalasia (which has NO known underlying cause, it is due to the failure of distal esophageal
inhibitory neurons)
+Secondary achalasia (occurs to other conditions, such as esophageal cancer or Chagas disease)
-Causes :
.lymphoma
.carcinoma
.chaga`s disease
.neurotropic viruses
.ischemia
.irradiation
.drugs and toxins
.postvagotomy
+The cause of most cases of achalasia is unknown
-Diagnosis :
.esophageal manometry
.barium swallow radiographic studies
.esophagogastroduodenoscopy EGD
-Treatment :
.pneumatic balloon dilation
.pneumatic dilation or surgery (surgical myotomy)
.botulinum toxin
By Dr.Mohammad abu sheikha@
-Treatment :
.nitroglycerin, calcium channel blockers (nifedipine, nitrates), hydralazine
.proton pump inhibitors PPIs
.botulinum toxin
**Esophagitis
-Is inflammation of the esophagus. It may be acute or chronic
-Causes :
.infectious (are typically seen in immunocompromised people) Types :
.Esophageal candidiasis M.C / Viral - Herpes simplex (Herpes esophagitis), Cytomegalovirus albicans
+M.C infection is from Candida
+Endoscopy can be used to distinguish among these conditions
.GERD (M.C.C)
.chemical injury by alkaline or acid solutions
.physical injury resulting from radiation therapy or by nasogastric tubes
.pill esophagitis
.hyperacidity
.alcohol abuse
.eosinophilic esophagitis
.esophageal carcinoma
.esophageal obstruction
.Crohn's disease – a type of IBD which is also an autoimmune disease where the immune system in flames the gastrointestinal
tract
.certain medications (doxycycline)
.smoking, alcohol
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.pregnancy
.surgery in achalasia
.Zollinger-Ellison syndrome
.high blood calcium level (hypercalemia)
.scleroderma and systemic sclerosis
.the use of medicines (prednisolone, tricyclic)
.visceroptosis or Glénard syndrome
+Factors that have been linked with GERD (but not conclusively) :
.obstructive sleep apnea
.gallstones
-Differential Diagnosis :
.chest pain such as heart disease
.respiratory and laryngeal signs and symptoms, is called laryngopharyngeal reflux (LPR) or "extraesophageal reflux disease"
(EERD). Unlike GERD, LPR rarely produces heartburn, and is sometimes called silent reflux
-Diagnosis :
.pH monitor (gold standard) (may be useful in those who do not improve after PPIs and is not needed in those in whom
Barrett's esophagus is seen)
+Investigation for H. pylori is NOT usually needed
-Treatment :
.PPIs (proton-pump inhibitors - omeprazole, esomeprazole, lansoprazole (will all reliably increase the PH of gastric contents)
.H2 blockers (should only be used in Pt. has very mild, intermittent symptoms)
-Complications :
.anemia (iron deficiency)
.recurrent chest infections
.esophagitis (M.C.C of esophagitis is GERD)
.pulmonary (aspiration pneumonia, cough and asthma)
.barrett's esophagus
.motility disturbances
.benign esophageal stricture
.esophageal Carcinoma
.gastric volvulus
.Esophageal dilatation
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.If it is caused by esophagitis, in turn caused by an underlying infection, it is commonly treated by treating the infection
(typically with antibiotics)
.H2 antagonist (e.g. ranitidine) or a proton-pump inhibitor (e.g. omeprazole) can treat underlying acid reflux disease
**Barrett's Esophagus
-The epithelium of the lower esophagus undergoes histologic change from a normal squamous epithelium to a columnar
epithelium (GERD for long time) / Refers to an abnormal change (metaplasia) in the cells of the lower portion of the esophagus
-Is a complication of long standing reflux disease. After several years of GERD
+The risk of developing Barrett's esophagus is increased by central obesity
-Signs & Symptoms :
.frequent and long standing heartburn
.trouble swallowing (dysphagia)
.vomiting blood (hematemesis)
.pain under the sternum (where the esophagus meets the stomach)
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-Diagnosis :
.endoscopy (Pt. with Barrett's Esophagus should have a repeat endoscopy every 2-3yrs to see whether dysplasia or esophageal
cancer)
.esophagectomy is warranted if high grade dysplasia is found
-Treatment :
.PPIs
**Hiatus Hernia
1.Oesophago-gastric hernia (Sliding)
.M.C type / Herniations of the cardia and very small part of the stomach through the diaphragm
.it is common in old age obese female (increase the intra-abdominal pressure)
2.Para-oesophageal hernia (Rolling)
.part of stomach (fundus) herniated through the diaphragm without herniations of the cardia
.usually there are no symptoms
3.Mixed hernia
+Esophageal web in Plummer-Vinson syndrome is found at upper end of esophagus (post cricoid region) and Schatzki ring may
be found at the lower end of esophagus
-Signs & Symptoms :
.dysphagia (difficulty in swallowing)
.pain
.weakness
.odynophagia (painful swallowing)
.atrophic glossitis
.angular stomatitis
.post-cricoid web
.iron deficiency
-Complications :
.developing squamous cell carcinoma of the oral cavity, esophagus, and hypopharynx
-Treatment :
.with iron supplementation, IF NOT;
.the web can be dilated during upper endoscopy to allow normal swallowing and passage of food
**Mallory-Weiss Syndrome
-Refers to bleeding from a laceration in the mucosa at the junction of the stomach and esophagus
+This is usually caused by severe vomiting because of alcoholism or bulimia, but can be caused by any conditions which causes
violent vomiting and retching such as food poisoning
+The syndrome presents with painful hematemesis. The laceration is sometimes referred to as a Mallory-Weiss tear
+Is a non transmural tear of the lower esophagus that is related to repeated episodes of retching and vomiting
+The tear involves mucosa and submucosa but not the muscular layer (contrast to Boerhaave syndrome which
involves all the layers)
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**Abdominal Pain
-Causes Of Chronic Or Recurrent Abdominal Pain :
.aortic aneurysm
.malignancy
.lymphadenopathy
.abscess
.depression
.anxiety
.hypochondriasis
.somatization
.DM
.addison's disease
.hypercalcemia
.drugs/toxins (corticosteroids, lead, alcohol, azathioprine)
.haematological (sickel-cell disease, haemolytic disorders)
.spinal cord lesions
.esophageal causes (spasm, GERD, oesophagitis)
.gastro-duodenal casues (overfeeding, gastritis, peptic ulcer)
.intestinal causes (UC-CD, diverticulitis, appendicitis, intestinal parasites, tuberculosis, obstruction-irritable colon)
.biliary causes (gallstones, cholecystitis)
.pancreatic causes
.hepatic causes
.urinary causes
.genital causes
.vascular casuses
**Vomiting
-Causes :
.CNS disorders (vestibular neuronitis, migraine, raised intracranial pressure, meningitis)
.gastroduodenal (PUD, gastric cancer, gastroparesis)
.uraemia
.the acute abdomen (appendicitis, cholecystitis, pancreatitis, intestinal obstruction)
.alcoholism
.drugs (NSAIDs, opiates, digoxin, antibiotics, cytotoxins)
.infections (hepatitis, gastroenteritis, UTI)
.metabolic (diabetic ketoacidosis, addison`s disease, cyclical vomiting syndrome, hyperglycaemia, hypoglycaemia ,acidosis,
alkalosis, hyperparathyroidism)
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**Gastritis
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-Inflammation, erosion or damage of the gastric lining that has not developed into an ulcer / Is inflammation of the lining of
the stomach. It may occur as a short episode or may be of a long duration
+Gastrin is produced primarily in the Pylorus
-Types :
+type A (autoimmune)
.gastritis from atrophy of the gastric mucosa and is associated with autoimmune processes, such as Vit B12 deficiency
.also linked to diminished gastric acid production and achlorhydria, and it is lead to gastric cancer
+Achlorhydria (production of hydrochloric acid in gastric secretions of the stomach and other digestive organs is absent or low)
+Hypochlorhydria Is Caused By :
.carcinoma of stomach
.pregnancy
.pernicious anemia
.atrophic gastritis
-Causes Of Gastritis :
.H.pylori (M.C.C of chronic gastritis)
.alcohol, smoking, cocaine abuse
.NSAIDs (aspirin)
.drugs as (iron preparation)
.radiation therapy
.autoimmune problems or disease (Crohns disease)
.sever stress as (burn, trauma, infection, surgery and organ failure)
-Complications :
.bleeding
.stomach ulcers
.stomach tumors
.low red blood cells due to not enough (vitamin B12) - a condition known as pernicious anemia
-Diagnosis :
.endoscopy (BEST)
.Presence of H. pylori
.blood cell count
.stool sample (to look for blood in stool)
-Treatment :
.PPIs
.H2 blockers
.antibiotics
acid-secreting cells of the stomach (parietal cells) to maximal activity, with consequent gastrointestinal mucosal
ulceration
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+Is hypergastrinemia caused by cancer of gastrin-producing cells (gastrinoma) – excessive production and release of
gastrin G cells
+The primary tumor associated with ZES is usually located in the pancreas (M.C site), duodenum, stomach or abdominal lymph
nodes, but ectopic locations have also been described (e.g., heart, ovary, gallbladder, liver, kidney)
+ZES may occur sporadically or as part of an autosomal dominant familial syndrome called multiple endocrine neoplasia type
1 (MEN 1)
+A small percentage are associated with parathyroid, pituitary and pancreatic tumors, anemia, chronic gastritis, renal failure,
hyperthyroidism
+Malignant tumors that most commonly spread to the liver and lymph nodes near the pancreas and small bowel
+Patients with gastrinomas have multiple tumors as part of a condition called multiple endocrine neoplasia type I (MEN I) - MEN
I patients have tumors in their pituitary gland and parathyroid glands, in addition to tumors of the pancreas
-Signs & Symptoms :
.abdominal pain and diarrhea
.chronic diarrhea, including steatorrhea (fatty stools)
.pain in the esophagus (especially between and after meals at night)
.nausea
.wheezing
.vomiting blood (digested blood)
.malnourishment
.loss of weight due to loss of appetite
-Diagnosis :
.endoscopy
+Laboratory Tests :
.secretin stimulation test, which measures evoked gastrin levels
.fasting gastrin levels, on at least three separate occasions
.gastric acid secretion and pH
.increased level of chromogranin A (is a common marker of neuroendocrine tumors)
+Normal basal gastric acid secretion is less than 10 mEq/hour, while in Zollinger–Ellison syndrome it is usually more than 15
mEq/hour
+The source of the increased gastrin production must be discovered. This is either done using MRI or somatostatin receptor
scintigraphy, the investigation of choice
-Treatment :
.PPIs (omeprazole, lansoprazole)
.H2 blockers (famotidine, ranitidine)
+Octreotide is the best drug for pharmacologic management. Cure is only possible if the tumors are surgically removed, or
treated with chemotherapy
+The pain caused by peptic ulcers can be felt anywhere from the navel up to the sternum, it may last from few minutes to
several hours and it may be worse when the stomach is empty
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-Causes :
.history of heartburn
.gastroesophageal reflux disease (GERD)
.medicines associated with peptic ulcer include (NSAIDs that inhibit cyclooxygenase) (glucocorticoids - dexamethasone,
prednisolone)
.H.pylori (60% of gastric and up to 50-75% of duodenal ulcers) (M.C.C)
.stress (it does not seem to independently increase risk. Even when coupled with H. pylori infection)
.dietary factors, such as (spice consumption, caffeine and coffee, alcohol, smoking) (it does not seem to independently increase
risk. Even when coupled with H. pylori infection)
.gastrinoma (Zollinger–Ellison syndrome), rare gastrin-secreting tumors, also cause multiple and difficult-to-heal ulcers
-Complications :
.gastrointestinal bleeding (M.C complication) (it occurs when the ulcer erodes one of the blood vessels, such as the
gastroduodenal artery)
.perforation (sign is Valentino's syndrome)
.penetration (is a form of perforation in which the hole leads to and the ulcer continues into adjacent organs such as the liver
and pancreas)
.gastric outlet obstruction (is the narrowing of pyloric canal by scarring and swelling of gastric antrum and duodenum due to
peptic ulcers / Patient often presents with severe vomiting without bile)
.cancer
-Differential Diagnosis :
.gastritis
.stomach cancer
.gastroesophageal reflux disease GERD
.pancreatitis
.hepatic congestion
.cholecystitis
.biliary colic
.inferior myocardial infarction
.referred pain (pleurisy, pericarditis)
.superior mesenteric artery syndrome
.people who are taking non steroidal anti-inflammatories (NSAIDs) may also be prescribed a prostaglandin analogue
(misoprostol) in order to help prevent peptic ulcers
.acid reducing medication (ranitidine and famotidine, which are both H2 receptor antagonists, provide relief of peptic ulcers,
heartburn, indigestion. They decrease the amount of acid in the stomach helping with healing of ulcers)
+In the absence of H. pylori, 4 weeks of a PPIs are also often used
.When H. pylori infection is present, the most effective treatments are combinations of 2 antibiotics (e.g. clarithromycin,
amoxicillin, tetracycline, metronidazole) and a proton-pump inhibitor (PPI)
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.In complicated, treatment-resistant cases, 3 antibiotics (e.g. amoxicillin + clarithromycin + metronidazole) may be used
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-Commoner than GU / M > F / The M.C pathophysiologic mechanism of DU is primarily related to (Gastric acid hypersecretion)
+Increased gastric acid secretion / increased gastric emptying / decreased duodenal pH
+Chronic duodenal ulcer usually occurs in the first part of the duodenum (bulb of duodenum) just distal to the junction of
pyloric and duodenal mucosa; 50% are on the anterior wall
-Signs & Symptoms :
.mid-epigastric pain, tenderness typically before meals at night, relieved by eating or drinking milk
.abdominal pain (in case of duodenal ulcers the pain appears about 3hrs after taking a meal , when the stomach begins to
release digested food and acid into the duodenum)
.nausea, vomiting
+Symptoms of duodenal ulcers would initially be relieved by a meal, as the pyloric sphincter closes to concentrate the stomach
contents, therefore acid is not reaching the duodenum
+Perforation (anterior duodenal ulcer) / Bleeding (posterior peptic ulcer)
-Risk Factors :
.H.pylori
.drugs (aspirin, NSAIDs, steroids)
.blood group O
.smoking
.cancer of stomach
.zollinger-ellison syndrome (syndrome must you always think of with a duodenal ulcer)
.crohns disease
.head truma
.hyperparathyroidism
.chronic pulmonary insufficiency
-Diagnosis :
.upper GI endoscopy
.sucralfate
.sismuth
.sirazepine
.H2-receptors antagonists
.old age (M > F) (Estrogen may protect women against the development of this cancer form)
.blood group A
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.H.pylori (M.C.C)
.autoimmune gastritis
.adenomatous gastric polyp
.GERD
.obesity
.smoking, alcohol
.iodine deficiency
.genetic risk factor for gastric cancer is a genetic defect of the CDH1 gene (E-cadherin, lies on the 16th chromosome) known as
hereditary diffuse gastric cancer (HDGC) (autosomal dominant)
.AIDS
.DM
.pernicious anemia
.chronic atrophic gastritis
.Menetrier's disease (hyperplastic, hypersecretory gastropathy)
.intestinal metaplasia
+A Mediterranean diet is also associated with lower rates of stomach cancer, as is regular aspirin use
+Sister mary joseph's sign is (periumbilical lymph node gastric cancer metastasis; present as periumbilical mass)
+Krukenberg's tumor is (gastric cancer or other adenocarcinoma, that has metastasized to the ovary)
+Irish`s node is (left axillary adenopathy from gastric cancer metastasis)
+Surveillance laboratory findings is (CEA elevated in 30% of cases)
+Histology (adenocarcinoma) / anus – esophagus (squamous cell carcinoma)
-Histologic Types :
.intestinal (glands)
.diffuse (no glands)
-Morphology Types :
.ulcerative (M.C morphologic type of gastric cancer)
.polypoid
.scirrhous
.superficial
.linitis plastica (leather bottle)
+Gastric cancer more common on the lesser curvatures / proximal gastric cancer is more common
-Gastric Adenocarcinoma Metastasize (spread to other sites in the body by metastasize) :
.hematogenously
.lymphatically
.90% are adenocarcinoma
.5% of gastric malignancies are lymphomas (M.C GI lymphoma)
.M.C site for GI lymphoma is stomach
.metastasis occurs in 80-90% of individuals with stomach cancer
.M.C site for metastasis is liver
-Diagnosis :
.upper endoscopy + biopsy
-Treatment :
.surgery
+Endoscopic mucosal resection (EMR) is a treatment for early gastric cancer (tumor only involves the mucosa)
+Endoscopic submucosal dissection (ESD), used to resect a large area of mucosa in one piece
.chemotherapy and/or radiation therapy
+5-FU (fluorouracil) or its analog capecitabine, BCNU (carmustine), methyl-CCNU (semustine) and doxorubicin (Adriamycin), as
well as mitomycin C, and more recently cisplatin and taxotere
+Crohn's disease and ulcerative colitis present with extra-intestinal manifestations (such as liver problems, arthritis,
skin manifestations and eye problems) in different proportions
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+Diagnosis is generally by assessment of inflammatory markers in stool followed by colonoscopy with biopsy of pathological
lesions
+Both treated with anti-inflammatory medications such as (mesalzmine , azathioprine, 6-mercaptopurine ‘6MP’)
+The way doctors can tell the difference between Crohn's disease and UC is the location and nature of the inflammatory
changes (Crohn's can affect any part of the gastrointestinal tract, from mouth to anus (skip lesions), although a majority of the
cases start in the terminal ileum) (Ulcerative colitis, in contrast, is restricted to the colon and the rectum)
*Crohn`s Disease CD
-Crohn's can affect any part of the GI tract, from mouth to anus (skip lesions), although a majority of the cases start in the
terminal ileum
-Crohn's disease affects the full thickness of the bowel wall (transmural lesions) / It is a chronic transmural granulomatous
inflammation
+Genetic factor (CARD 15/NOD-2) mutations predispose / More common in smokers / Colon cancer (Slight) (UC > CD)
+ASC Abx (anti-saccharomyces cerevisiae antibodies) are associated with CD / Cytokine response - Associated with Th17
+CD is more likely to be associated with a palpable abdominal mass because CD has granulomas in the bowel wall
+Caused by a combination of environmental, immune and bacterial factors in genetically susceptible individuals
+CD can result in (vitamin B12 ,calcium ,vitamin K and iron deficiencies because of malabsorption)
+Prothrombin time PT may be prolonged in CD because of Vit K malabsorption
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+Kidney stones form more often in CD because the fat malabsorption results (in a low calcium level and an increased
absorption of oxalate, which forms kidney stones)
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-Complications :
.perforation, fistula
.intestinal obstruction
-Investigations :
.colonoscopy and biopsy
.barium (show string sign)
.in children fecal calprotectin is useful
Crohn's histology :
- Inflammation occurs in all layers, down to the serosa --> strictures, fistulas, adhesions etc
- Oedema of mucosa and submucosa, combined with deep fissured ulcers
- 'rose-thorn' --> 'cobblestone' pattern
- Lymphoid aggregates
- Non-caseating granulomas
*Ulcerative Colitis UC
-That causes inflammation and ulcers in the colon. It may affect just in the rectum (Colon and rectum only) – large bowel, it is
exclusively a mucosal disease / Ulcerative colitis is restricted to the mucosa (epithelial lining of the gut)
-Genetic factor (HLA-DR103) associated with severe disease / More common in non-smokers / M > F / Colon cancer (common-
Considerable) (UC > CD)
-ANC Abx (anti-neutrophil cytoplasmic antibody) is associated with UC / Cytokine response - Vaguely associated with T h2
.anemia (Vit B12 deficiency - are NOT because at duodenum / only in CD)
.weight loss (rare in UC) (CD > UC)
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.clubbing
.rheumatologic disease (ankylosing spondylitis, sacroiliac joint, joints-arthritis, erythema nodosum, arthropathy)
.pyoderma gangrenosum
.conjunctivitis
.sacroilitis, osteomalacia
.fatty liver
.renal stones (more in CD)
.amyloidosis
.bile duct involvement (cholangitis)
Histology
- ('pseudopolyps')
- Inflammatory cell infiltrate in lamina propria
- Crypt abscesses neutrophils migrate through the walls of glands to form depletion of goblet cells and mucin
from gland epithelium
- Granulomas are infrequent
+TREATMENT :
.Mesalazine Less useful (CD) More useful (UC)
.Antibiotics Effective in long-term (CD) Generally not useful (UC)
.Surgery Often returns following removal of affected part (CD)
Usually cured by removal of colon (UC)
+IBD may require immunosuppression to control the symptom, such as prednisone, TNF inhibition, azathioprine (Imuran),
methotrexate, or 6-mercaptopurine
+Severe cases may require surgery, such as bowel resection, strictureplasty or a temporary or permanent colostomy or
ileostomy
+Ulcerative colitis can in most cases be cured by proctocolectomy
+Upper endoscopy (Are NOT)
+Both are most accurately DIAGNOSED with endoscopy
+Both are TREATED with anti-inflammatory medications (mesalamine, azathioprine, 6-mercaptopurine 6MP, steroids)
+Both forms of IBD can lead to colon cancer after 8-10 years of involvement of the colon (UC > CD)
+Definite diagnosis of inflammatory bowel diseases by colonoscopic findings
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+Diagnostic Findings CD UC
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**Diarrhea
-Having three or more loose or liquid stools per day, or as having more stools than is normal for that person / Increased stool
water (>200mL/daily)
+Exudative diarrhea, occurs with the presence of blood and pus in the stool. This occurs with inflammatory bowel diseases,
such as Crohn's disease or ulcerative colitis, and other severe infections such as E. coli or other forms of food poisoning
+Inflammatory diarrhea, occurs when there is damage to the mucosal lining or brush border, which leads to a passive loss of
protein-rich fluids and a decreased ability to absorb these lost fluids. It can be caused by bacterial infections, viral infections,
parasitic infections, or autoimmune problems such as inflammatory bowel diseases. It can also be caused by tuberculosis, colon
cancer, and enteritis
+Dysentery diarrhea, if there is blood visible in the stools, it is also known as dysentery. The blood is trace of an invasion of
bowel tissue. Dysentery is a symptom of, among others, Shigella, Entamoeba histolytica, and Salmonella
+Pts. who present with a history of diarrhea lasting more than 10 days rarely have an infective cause
+If the Pt. is hypotensive, febrile and having abdominal pain, (Pt.) should be admitted to the hospital and given intravenous
fluids and antibiotics / The presence of blood in the stool is especially serious ans is probably the single strongest indication for
the use of antibiotics, such as ciprofloxacin
+Acute Diarrhea
.viral gastroenteritis with rotavirus
.travelers however bacterial infections predominate
.various toxins such as mushroom poisoning
.drugs (antibiotics, cytotoxic drugs, PPIs and NSAIDs)
+Chronic Diarrhea
.IBS (M.C.C of chronic or relapsing diarrhea)
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.amoebic colitis
.cancer colon (carcinoma) - colonic neoplasia
.diverticulosis
.malabsorption
.hyperthyroidism-thyrotoxicosis
.lactose-intolerance
.DM
.carcinoid syndrome
.Zollinger-Ellison syndrome
.food poisoning
.Zinc deficiency
.Vit A deficiency
.lincomycin intake
+Ulcerative colitis is marked by chronic bloody diarrhea and inflammation mostly affects the distal colon near the rectum
+Crohn's disease typically affects fairly well demarcated segments of bowel in the colon and often affects the end of the small
bowel
*Infectious Diarrhea
-The M.C.C of infectious diarrhea are campylobacter and salmonella, especially in Pts. with sickle cell and achlorhydria
-Causative Agent :
.campylobacter (reactive arthritis, Guillain-Barre` Syndrome – M.C.C)
.cryptosporidium, isospora (found in HIV-positive Pts.)
.E.coli (associated with the ingestion of contaminated hamburger meat – the organism can releases a shiga toxin, hemolytic
uremic syndrome)
.giardia (the ingestion of unfiltered water – is best diagnosed with ELISA stool antigen test and treated with metronidazole -
never gives blood in the stool, there is abdominal fullness, bloating and gas – can also stimulate celiac disease)
.salmonella (ingestion of chicken and eggs)
.scombroid (Pts. who ingest contaminated fish experience vomiting, diarrhea, flushing)
.shigella, yersinia (yersinia can mimic appendicitis, also common in people with iron overload, hemochromatosis)
.vibrio parahaemolyticus
.vibrio vulnificus
.viral
.staphylococcus aureus (ingestion of dairy products, eggs, salads, short incubation period 1-6hrs, upper GI symptoms –nausea,
vomiting, rarely diarrhea)
.ciguatera-toxin (2-6hrs after ingestion of large reef fish, also neurological symptoms)
+Giardiasis-Cholera (watery diarrhea)
.yersinia enterocolitica
.cholera
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.clostridium
+Viral
.rotavirus (M.C.C of viral diarrhea in children under five years old)
.norovirus (M.C.C of viral diarrhea in adults)
.adenovirus (types 40, 41)
.astroviruses
.norwalk virus
.enterovirus
+Parasites
.balantidium coli
.helminth (ascaris lumbricoides, ancylostoma duodenale, strongyloides)
.protozoa (Cryptosporidium spp., Giardia spp., Entamoeba histolytica, Blastocystis spp., Cyclospora cayetanensis)
+Are frequently the cause of diarrhea that involves chronic infection
+The broad-spectrum antiparasitic agent nitazoxanide has shown efficacy against many diarrhea-causing parasites
+Nitazoxanide is a broad-spectrum antiparasitic and broad-spectrum antiviral drug that is used in medicine for the treatment of
various helminthic, protozoal, and viral infections. It is indicated for the treatment of infection by Cryptosporidium parvum and
Giardia lamblia in immunocompetent individuals and has been repurposed for the treatment of influenza
+H.pylori (are NOT)
*Antibiotic-Associated Diarrhea
-M.C.C of diarrhea secondary to antibiotic use is Clostridium Difficile (any antibiotic can lead to diarrhea with C.difficile,
although clindamycin may have one of the highest frequencies of association)
-Treatment :
.metronidazole (is drug of choice)
.oral vancomycin (is only to be used in the very occasional case that does not resolve with metronidazole)
(taurocholic acid - is a drug used in a clinical test to diagnose bile acid malabsorption)
*Carcinoid Syndrome
-Describes tumors of the neuroendocrine syndrome. They are most often located in the appendix and the ileum
-Signs & Symptoms :
.diarrhea
.flushing
.tachycardia
.hypotension
.rash (from niacin deficiency-serotonin and niacin are both produced from tryptophan. If there is an overproduction of
serotonin, it produces a tryptophan deficiency, which lead to a deficiency of niacin)
.endocardial fibrosis (because of a constant exposure of the right side of the heart to the serotonin)
.can lead to tricuspid insufficiency and pulmonic stenosis
-Diagnosis :
.urinary 5-hydroxyindoleacetic acid level (5-HIAA)
*Malabsorption
-Causes :
.enzyme deficiencies or mucosal abnormality, as in food allergy and food intolerance, e.g. celiac disease (gluten intolerance),
lactose intolerance (intolerance to milk sugar) and fructose malabsorption
.pernicious anemia, or impaired bowel function due to the inability to absorb vitamin B12
.loss of pancreatic secretions, which may be due to cystic fibrosis or pancreatitis
.structural defects, like short bowel syndrome (surgically removed bowel) and radiation fibrosis, such as usually follows cancer
treatment and other drugs, including agents used in chemotherapy
.certain drugs, like orlistat, which inhibits the absorption of fat
-Causes :
.Giardia lamblia
.Celiac disease
.Pancreatic insufficiency
.Intestinal lymphoma
.Crohn's disease
.Gluten enteropathy
.Systemic sclerosis
.Bacterial overgrowth
.Lymphoma
.Tropical sprue
.Systemic sclerosis
.Pancreatic carcinoma
.Diverticula
.radiation enteritis
.HIV
.Parasites (giardia lamblia, fish tape worm, roundworm)
.gastroenteritis
.Short bowel syndrome
.Gastrectomy, vagotomy
.Lactose intolerance
.Cystic fibrosis
.Chronic pancreatitis (NOT acute)
**GI Bleeding
*Upper Gastrointestinal Bleeding (UGIB)
-Bleeding arising from the esophagus, stomach, or duodenum
-Blood may be observed in vomit (hematemesis) or in altered form in the stool (melena)
-Signs & symptoms :
.hematemesis
.coffee ground vomiting
.melena, or hematochezia (maroon coloured stool) if the hemorrhage is severe
+Glasgow-Blatchford score (the Glasgow-Blatchford bleeding score (GBS) is a screening tool to assess the likelihood that a
patient with an acute upper gastrointestinal bleeding (UGIB) will need to have medical intervention such as a blood transfusion
or endoscopic intervention)
-Score (score is equal to "0" if the following are all present) :
.Hemoglobin level >12.9 g/dL (men) or >11.9 g/dL (women) (for men; 12.0-12.9 1 / 10.0-11.9 3 / <10.0 6)
(for women; 10.0-11.9 1 / <10.0 6)
.Systolic blood pressure >109 mm Hg (100–109 1 / 90–99 2 / <90 3)
.Pulse <100/minute
.Blood urea nitrogen level <18.2 mg/dL (6.5-8.0 2 / 8.0-10.0 3 / 10.0-25 4 / >25 6)
.No melena or syncope
.No past or present liver disease or heart failure
Other markers
.Pulse ≥100 (per min) 1
.Presentation with melaena 1
.Presentation with syncope 2
.Hepatic disease 2
.Cardiac failure 2
.angiodysplasia
.neoplasm — cancer
.diverticular disease (diverticulosis - M.C.C, diverticulitis)
.anal fissures
.rectal foreign bodies
.crohn's disease
.pseudomembranous colitis
.infectious diarrhea
.radiation colitis
.mesenteric ischemia
.colonic polyps
.colon cancer
-Diagnosis :
.eandoscopy, flexible sigmoidoscopy, colonoscopy, rarely barium enema
+Melena is four-times more likely to come from an upper gastrointestinal bleed than from the lower GI tract; however, it can
also occur in either the duodenum and jejunum, and occasionally the portions of the small intestine and proximal colon
-Causes :
.peptic ulcer disease (M.C.C)
.sign of drug overdose if a patient is taking anticoagulants, such as warfarin
.tumors, especially malignant tumors affecting the esophagus, more commonly the stomach & less commonly the small
intestine
.hemorrhagic blood diseases (e.g. purpura & hemophilia)
.gastritis
.esophageal varices
.aorto-duodenal fistula
.Meckel's diverticulum
.Mallory-Weiss syndrome
.iron supplements, Pepto-Bismol, Maalox, and lead
26
+Hematochezia - Bright red stool, is the sign of a fast moving active GI bleed. The bright red or Maroon color is due to the
short time taken from the site of the bleed and the exiting at the anus. The presence of hematochezia is six-times greater in a
LGIB than with a UGIB
-Causes :
.hemorrhoids and diverticulosis (M.C.C)
.colorectal cancer, which is potentially fatal
.in a newborn infant, haematochezia may be the result of swallowed maternal blood at the time of delivery, but can also be an
initial symptom of necrotizing enterocolitis
.in babies, haematochezia in conjunction with abdominal pain is associated with intussusception
.in adolescents and young adults, inflammatory bowel disease, particularly ulcerative colitis, is a serious cause of
haematochezia that must be considered and excluded
.crohns disease
.other types of inflammatory bowel disease, inflammatory bowel syndrome, or ulceration
.rectal or anal hemorrhoids or anal fissures
.shigella or shiga toxin producing E. coli food poisoning
.necrotizing enterocolitis
.salmonellosis
**Portal Hypertension
-Is hypertension (high blood pressure) in the hepatic portal system, which is composed of the portal vein and its branches and
tributaries. Portal hypertension is defined as elevation of hepatic venous pressure gradient
-Portal pressure gradient (the difference in pressure between the portal vein and the hepatic veins)
-Normal portal pressure is generally defined between (5-10mm Hg) / Complications do not usually develop until the portal
venous pressure exceeds 12mmHg
-Complications :
.portacaval anastomoses (esophageal variceal bleeding, gastric varices, anorectal varices, caput medusae)
.abdominal tenderness (spontaneous bacterial peritonitis; causes-liver cirrhosis, ascites, E.coli-due to spontaneous
bacter/treated by antibiotic-ceftriaxone)
.carcinoma
.congestive gastropathy
.iron deficiency anemia
.renal failure
.jaundice (Hepatorenal syndrome)
27
-Diagnosis :
.HVPG (hepatic venous pressure gradient)
-Treatment :
+Prophylaxis of variceal bleeding (B-blocker like propranolol and isosorbide mononitrate) (endoscopic – banding ligation)
+TIPS (transjugular intrahepatic portosystemic shunting) to reducing rate of rebleeding (Disadvantages of TIPS include, high
cost, increased risk of hepatic encephalopathy)
+Management Of Ascites :
.salt restriction
.diuretics (spironolactone)
.paracentesis
.TIPS
.peritoneovenous shunt (LeVeen Shunt - is a shunt which drains peritoneal fluid from the peritoneum into veins)
+For control of hepatic encephalopathy (dietary protein, followed by lactulose, use of oral antibiotics like neomycin)
**Viral Hepatitis
+All hepatitis virus types are (RNA), except HBV is (DNA) / A-B (only have vaccine)
*Hepatitis A
-Infectious jaundice is caused by hepatitis A virus / Antibodies (HAV IgM) / Incubation 2-4wks (15-45days) / Severity (mild-
acute)
-Markers (IgM anti HAV in acute infection / IgG anti HAV in old infection)
+Its acute form and does not have a chronic stage (A-E)
-Transmission :
.fecal-oral route
.associated with ingestion of contaminated food
+A vaccine is avaliable that will prevent HAV infection for up to 10yrs (Vaccine is protection for 10yrs)
+Infected people excrete HAV with their feces 2wks before and 1wks after the appearance of jaundice
+Symptoms less in children than adults
*Hepatitis B
-Incubation 6wks-6months (45-160days) / Antibodies HBsAg, HBeAg (highly infectious-chronic active) / Severity (chronic-severe)
-HBV-DNA by PCR technique (is the most sensitive test) / Vaccine is protection for 15yrs or lifelong immunity – 3 doses
-Transmission :
.blood (blood transfusion)
.tattoos
.sexually (sexual intercourse or through contact with blood or bodily fluids)
.via mother to child by breast feeding
28
-Comlications :
.chronic hepatitis (develops in 15% of adults)
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.cirrhosis
.hepatocellular carcinoma (after 30yrs)
-Treatment :
.alpha-interferon
*Hepatitis C
-No vaccine / Incubation 2-26wks (15-150days) / Antibodies (Core antigen) / Severity (chronic) / NO vaccine
-Markers HCV AB-appear after 3-6 months of infection
-HCV-RNA by PCR technique is the most sensitive test
-Transmission :
.blood
.saliva
-Complications :
.chronic hepatitis
.cirrhosis (after 15-20yrs)
+It usually remains asymptomatic
-Treatment :
.interferon
.antiviral drug ribavirin
*Hepatitis D
-It can only propagate in the presence of the hepatitis B virus / Antibodies (Delta antigen) / Incubation 6-9wks (30-60days) /
Severity (exacerbated symptoms of HBV; chronic HBV) / NO vaccine
-Markers (IgM in acute infection / IgG in chronic infection / hepatitis B marker in positive)
-Transmission :
.blood (blood transfusion)
.tattoos
.sexually (sexual intercourse or through contact with blood or bodily fluids)
.via mother to child by breast feeding
*Hepatitis E
-The hepatitis E virus (HEV) produces symptoms similar to hepatitis A / Incubation 3-8wks (15-60days) / Severity (normal Pt. –
acute, mild) (Pregnant women – severe) / NO vaccine
+Its acute form and does not have a chronic stage (A-E)
-It can take a fulminant course in some Pts. (pregnant women)
-Markers (IgM in acute infection / IgG in old infection)
-Transmission :
.oral
**Chronic Hepatitis
-Chronic inflammatory reaction in liver more than 6 months
-Causes :
.viral hepatitis B-C-D
+Its acute form and does not have a chronic stage (A-E)
.drugs
.autoimmune hepatitis
.wilson`s disease
.hemochromatosis
.alpha-1 antitrypsin
.statins
.hydralazine
.methyldopa
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+These medications can also cause acute hepatitis or an autoimmune hepatitis like syndrome
-Clinical :
.asymptomatic (it may be discover accidental aselevation of liver enzymes)
.mild non-specific symptoms as (easy fatigue, malaise, anorexia and weight loss)
.jaundice (yellowish coloration of skin and mucous membrane, pale stool and dark urine)
.other liver cell failure manifestations as oedema, ascites, bleeding tendency and encephalopathy
.in late case liver cirrhosis with (liver cell failure, portal hypertension, hepatocellular carcinoma)
.extrahepatic symptoms (rash, urticaria, arthritis, glomerulonephritis, lymphocytic sialadenitis, poly arteritis nodosa PAN,
polyneuropathy, porphyria)
-Treatment :
1.interferon – indications (no cirrhosis, young age, elevated enzymes, biopsy evidence of chronic hepatitis, in case of hepatitis
B-C)
+Dose (HBV-5 million units daily at least 4 months) (HCV-3 million units 3 times/week for 12-18 months)
+Side effects (bone marrow depression, autoimmune disease, CNS syndrome, anorexia, sleep disturbance)
2.antiviral drugs (HBV-lamivudine or famciclovir, alone without interferon for 12months) (HCV-ribavirin with interferon)
+Chronic hepatitis interferes with hormonal functions of the liver which can result in acne, hirsutism
(abnormal hair growth), and amenorrhea (lack of menstrual period) in women
+Cirrhosis can lead to other life-threatening complications such as hepatic encephalopathy, esophageal varices, and
hepatorenal synrome
*Autoimmune Hepatits
-Is a disease of the liver that occurs when the body`s immune system attacks cells of the liver
-Types :
.associated with anti smooth muscle AB and anti nuclear AB
.associated with anti liver-kidney microsomal AB
-Signs & Symptoms :
.F > M (young-middle age)
.fatigue, amenorrhea
.cirrhosis, low albumin, spider nivae, elevated serum aminotransferase levels (ALT-AST) (signs of chronic liver disease)
.progressive jaundice, fever, painful hepatomegaly (signs of acute hepatitis)
.hereditary hemochromatosis
.skin hyperpigmentation
.extrahepatic manifestations (rash, arthritis, thyroiditis, haemolytic anemia and glomerulonephritis)
.DM
.pseudogout
.cardiomyopathy (all signs due to iron overload)
-Diagnosis :
.elevated serum aminotransferase levels (elevated ALT, AST)
.liver function tests (in 50% of Pts., abnormal results – decreased albumin levels, PPT)
.liver biopsy
.antibodies found in blood (antinuclear antibody ANA, anti-smooth muscle antibody ASMA, liver/kidney microsomal antibody
LKM-1, LKM-2, LKM-3, anti soluble liver antigen SLA/LP and antimitochondrial antibody AMA)
-Treatment :
.immunosuppressive glucocorticoids steroids with or without prednisolone / azathioprine
+The combination of neurological symptoms, Kayser-Fleischer rings and a low ceruloplasmin level is considered sufficient for
Page
the diagnosis of Wilson's disease / Serum copper is low / Urine copper is elevated in Wilson's disease
-Signs & Symptoms :
.liver disease (cirrhosis)
.neuropsychiatric symptoms (about the half the people with Wilson's disease have neurologic or psychiatric symptoms)
.extrapyramidal syndrome (parkinsonism, ataxia, dystonia, tremor, demontia). Other neurological manifestations as seizures
and migraine and pschiatric manifestations as behavioral change, depression, anxiety, psychosis, altered mental status
.eyes (Kayser-Fleischer rings – KF rings), a pathognomonic sign, may be visible in the cornea of the eyes
+KF signs - greenish brown pigmentation at the the corneoscleral junction
.kidneys (renal tubular acidosis, aminoaciduria - presence of amino acids in the urine)
.heart (cardiomyopathy)
.hormones (hypoparathyroidism - failure of the parathyroid glands leading to low calcium levels, infertility, abortion)
.haemolytic anemia
-Characterized by :
.liver disease and neuropsychiatric symptoms are the main features that lead to diagnosis
.symptoms usually appear between the ages of 6 and 20 years
.failure of both binding of copper with apo ceruloplasmin and copper excretion in the bile, wich leading to deposition of copper
in liver and other tissue
.low serum ceruloplasmin level
+Ceruloplasmin - is a ferroxidase enzyme that in humans is encoded by the CP gene / is the major copper-carrying protein in
the blood, and in addition plays a role in iron metabolism
.increase hepatic copper content on liver biopsy
-Investigations :
.liver biopsy is the best
.ceruloplasmin is usually low
.total serum copper is usually low
.free serum copper is usually increased (>25 ug/dl)
.urinary copper is usually elevated (>100ug/dl)
.MRI (to show basal ganglia affection-giant panda sign)
.urine analysis and renal function test
.genetic testing
-Treatment :
.diet low in copper-containing foods is recommended with the avoidance of (mushrooms, nuts, chocolate, dried fruit, liver,
shellfish)
.penicillamine (1st treatment used – copper chelating), zinc acetate
.liver transplantation (effective cure for Wilson's disease)
.COPD
.asthma
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.pneumothorax
.gallstones
.pancreatitis
.autoimmune hepatitis
.glomerulonephritis
.pelvic organ prolapse
.bronchiectasis
.emphysema
.cancers (lymphoma, hepatocellular carcinoma-liver, lung cancer, gallbladder cancer, bladder carcinoma)
+Severe A1AT deficiency causes panacinar emphysema - Panlobular emphysema or COPD in adult life in many people with the
condition (especially if they are exposed to cigarette smoke)
-Diagnosis :
.level of AAT in your blood (low AAT levels)
.genetic test is the most certain way to check for AAT deficiency
.lung-related tests (lung function tests / CT scan)
+AAT Genetic testing is also recommended if you have a relative who has been diagnosed with A1AD or a family history of early
emphysema or liver disease
-Treatment :
.intravenous infusion of alpha 1-antitrypsin
.transplantation of the liver
**Hepatic Encephalopathy HE
-Is the occurrence of confusion, altered level of consciousness, and coma as a result of liver failure
+In the advanced stages it is called hepatic coma or coma hepaticum. It may ultimately lead to death
-Types :
.type A (acute) describes hepatic encephalopathy associated with acute liver failure, typically associated with cerebral edema
.type B (bypass) is caused by portal-systemic shunting without associated intrinsic liver disease
.type C (cirrhosis) occurs in patients with cirrhosis - this type is subdivided in episodic, persistent and minimal encephalopathy
-Signs & Symptoms :
.mild confusion, and irritability
.inverted sleep-wake pattern (sleeping by day, being awake at night) (the first stage of hepatic encephalopathy)
.lethargy and personality changes (the second stage)
.worsened confusion (the third stage)
.progression to coma (the fourth stage)
.asterixis
.neurological examination (clonus and positive Babinski sign)
.coma and seizures represent the most advanced stage
.cerebral edema (swelling of the brain tissue) leads to death
.jaundice
.ascites
.peripheral edema (swelling of the legs due to fluid build-up in the skin)
.tendon reflexes
-Causes :
.barbiturate
32
.morphine
.diuretic therapy
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+Some disorders do not normally cause haemochromatosis on their own, but may do so in the presence of other predisposing
factors. These include cirrhosis (especially related to alcohol abuse), steatohepatitis of any cause, porphyria cutanea tarda,
prolonged haemodialysis, and post-portacaval shunting
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-Diagnosis :
.serum ferritin elevated
.liver biopsy (BEST) Perl's stain
.Molecular genetic testing for the C282Y and H63D mutations
+Untreated develop due to hepatocullular carcinoma (Tumor marker is alpha fetoprotein AFP)
-Treatment :
.deferoxamine (iron-chelating)
+Human hemochromatosis protein HFE gene associated with HLA-A3
**Celiac Disease (Gluten enteropathy)
-Is an autoimmune disorder of the small intestine that occur in genetically predisposed people of all ages from middle infancy
onward / F > M
-Coeliac disease is associated with other human leukocyte antigen (HLA-DO2)-linked autoimmune disorders
+It can present at any age with positive family history in 25% of cases
-Signs & Symptoms :
.diarrhea
.weight loss
.anemia (iron deficiency anemia, folat anemia, Vit B12, megaloblastic anemia)
.malabsorption
.oral ulceration
.osteoporosis
.dermatitis herpetiformis
.growth failure
.hypocalcemia
.hyposplenism
(disease can cause it - celiac disease, UC, sickle cell anemia-autosplenectomy)
.Vit D malabsorption
.IgA deficiency
.adenocarcinoma (small intestine cancer and lymphoma of the small bowel)
-Complications :
.increased incidence of T cell lymphoma
.increased incidence of carcinoma of small intestine and oesophagus
-Diagnosis :
.intestine biopsy (duodenal biopsy – BEST)
.response to gluten-free diet
.antiendomysial antibodies on the immunoglobulin A (IgA) + antimicrosomal
-Treatment :
.life-long gluten-free diet
.dyspnea
.hypotension
.jaundice
.abnormal lung sounds - Crackles
.discoloration of abdominal wall – Turner’s or Cullen’s sign / fox sign
+Epigastric pain that radiates to back and relieved by leaning forward – aggravated by lying supine
-Causes : GET SMASHED
.gallstones (M.C of acute pancreatitis)
.scorpion bite (the least common cause)
.idiopathic
.ethanol (alcohol abuse)
.trauma
.mumps virus (coxsackievirus)
.autoimmune
.steroids
. Hypertriglyceridaemia, Hyperchylomicronaemia, Hypercalcaemia, Hypothermia , hyperlipidemia .
.ERCP
.diuretics (thiazide)
.azathioprine (immunosuppressive drug) - used in organ transplantation and autoimmune diseases
. mesalazine
-Diagnostic (Lap Tests) :
.CBC (high WBC)
.LFT
.elevated amylase and lipase
.CT-scan / abdomen ultrasound
.ABG
.calcium
.chemistry
.coags
.serum lipids
.RBS
.KFT
.LDH
-Complications :
.pseudocyst – resolve spontaneously by 6wks (M.C complication) (M.C indication for surgery in acute pancreatitis)
.infection and sepsis (M.C.C if death in acute pancreatitis)
.pancreatic necrosis, abscess
.pancreatic hemorrhage
.splenic / mesenteric / portal vessel rupture or thrombosis
.pancreatic ascites
.pancreatic pleural effusion (left)
.DM (type 1)
.ARDS / sepsis / MOF (multiple organ failure)
.coagulopathy
.encephalopathy (NH3) (treated by lactulose)
.severe hypocalcemia
.acidosis
.shock
-Treatment :
.NPO (non per oral)
.I.V fluids
.antibiotics
.analgesia
.if the cause is gallstone (cholycystectomy should be done once patient stabilized)
.pancreatic enzyme supplements
*Chronic Pancreatitis
-Is a long-standing inflammation of the pancreas that alters the organ's normal structure and functions. It can present as
episodes of acute inflammation in a previously injured pancreas, or as chronic damage with persistent pain or malabsorption
-Signs & Symptoms :
.epigastric pain
.malabsorption, diarrhea (steatorrhea)
.DM
.skin pigmentation (over the abdomen and back-flank)
.jaundice (obstructive)
+Chronic pancreatitis (Risk for pancreatic cancer)
+Pain may be relieved by leaning forwards or by drinking alcohol
-Causes :
.alcohol abuse (M.C.C)
.idiopathic
+Complications is associated with splenic vein thrombosis is (Gastric varices - treatment with splenectomy)
-Diagnosis :
.CT-scan (Best)
36
-Treatment :
.analgesia
Page
+Cullen`s Sign (Bluish discoloration of the periumbilical area from retroperitoneal hemorrhage)
+Grey Turner`s Sign (Ecchymosis or discoloration of the flank in Pts. with retroperitoneal hemorrhage from dissecting blood
from the retroperitoneum)
+Fox's Sign (Ecchymosis of the inguinal ligament from blood tracking from the retroperitoneum and collecting at the inguinal
ligament)
**Pancreatic Pseudocyst
-Encapsulated collection of pancreatic fluid
-Wall is formed by inflammatory fibrosis, Not epithelial lining
-Associated Risk Factors :
.chronic pancreatitis > acute pancreatitis
.pancreatitis from alcohol
+Chronic pancreatitis (alcohol) / Acute pancreatitis (gallstone)
+M.C.C of pancreatic pseudocyst is (Chronic alcoholic pancreatitis)
-Treatment :
.drainage of the cyst or observation
+M.C.C of death due to pancreatic pseudocyst is (Massive hemorrhage into the pseudocyst)
**Pncreatic Carcinoma
-Adenocarcinoma of the pancreas arising from duct cells
+Percentage arise in the pancreatic head is (66% in the head / 33% arise in the body and tail)
-Signs & Symptoms :
.painless jaundice
.pruritus
.courvoisier`s sign (Palpable, nontender, distended gallbladder)
.back pain
-Metastatic lymph nodes described classically for gastric cancer can be found with metastatic pancreatic cancer :
.virchow`s node (Lt. side)
.sister mary joseph`s nodule (per umbilicus)
+Tumor markers (pancreatic cancer) is (CA-19-9)
**Colorectal Carcinoma
-Adenocarcinoma of the colon or rectum
-Incidence :
.M.C GI cancer
(Female : lung cancer / breast cancer / colon cancer)
(Male : prostate cancer / lung cancer / colon cancer)
(M-F : lung cancer / colon cancer)
.second M.C.C of cancer deaths
.second M.C internal malignancy
.incidence increase with age starting at 49yrs and peaks at 70-80yrs
-Signs & Symptoms :
.weight loss (late sign)
.blood in the stool
.constipation
.change in bowel habit (if associated with bleeding)
.rectal bleeding
.anemia (iron-deficiency anemia)
+Lynch`s Syndrome (Hereditary nonPolyposis Colorectal Cancer / autosomal-dominant / inheritance of high risk for
development of colon cancer / 100% malignant)
-Diagnostic Test Is (colonoscopy / CBC / heme occult)
.via tumor biopsy, typically done during sigmoidoscopy or colonoscopy
38
+Microcytic anemia signify until proven otherwise in a man or postmenopausal women in colon cancer
+Preoperative workup for colorectal cancer is (CEA) carcinoembryonic antigen.
Page
-TNM stages :
.stage 1 (invades submucosa or muscularis propria)
.stage 2 (invades through muscularis propria or surrounding structures but with negative nodes)
.stage 3 (positive nodes, no distant metastasis)
.stage 4 (positive distant metastasis)
-Treatment :
.resection (surgical margins are needed for colon cancer is- >5cm (you should take as minimum 5cm); the minimum safety
margins in colectomy must be at least 2cm)
.chemotherapy (for advanced disease)
.NO radiotherapy in colon cancer
-Prevention :
.increasing the consumption of whole grains, fruits and vegetables
.reducing the intake of red meat
.aspirin and celecoxib (decrease the risk of colorectal cancer in those at high risk)
.Vit D intake
-Screening (three main screening tests) :
.fecal occult blood testing
.flexible sigmoidoscopy
.colonoscopy
+Carcinoma Of The Rectum usually causes early bleeding, mucus discharge or a feeling of incomplete emptying. Some of Pts
present with iron deficiency anemia or weight loss, on examination there may be a palpable mass ,hepatomegaly from
metastases
+Histology and cancer potential of an adenomatous polyp (villous > tubulovillous > tubular)
+Most polyps are found in (rectosigmoid)
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+Size Of Polyp :
.<1cm (<1% risk of cancer)
.1cm (10% risk of cancer)
.2cm (15% risk of cancer)
-Diagnosis :
.Colonoscopy
-Treatment :
.removal of polyp during colonoscopy
.prophylactic (colectomy)
**Polyposis Syndromes
*Familial Adenomatous Polyposis (FAP)
-Familial adenomatous polyposis FAP - Autosomal dominant
+Mutation on chromosome 5 – APC gene - Genetic defect (tumor marker) is (APC-adenomatous polyposis coli) gene
-Characteristics :
.100% malignant
.hundreds (>100) of adenomatous polyps within the rectum and colon
.developing at puberty (start at young age) / all undiagnosed; untreated Pts. develop cancer by ages 40-50 yrs
-Treatment :
.total proctocolectomy and ileostomy
.total colectomy and rectal mucosal removal (mucosal proctectomy) and ileoanal anastomosis
+With FAP, other tumor must be looked for is (duodenal tumors)
*Gardner`s Syndrome
-Autosomal dominant
-Characteristics :
.100% malignant
.neoplastic (adenomatous) polyps of the small bowel and colon
.cancer by age 40yrs in 100% of undiagnosed Pts., as in FAP
-Other Associated Findings :
.osteomas of skull (seen on x-ray)
.sebaceous cyst
.adrenal and thyroid tumors (Desmoid tumor)
-Treatment :
.total proctocolectomy and ileostomy
.total colectomy and rectal mucosal removal (mucosal proctectomy) and ileoanal anastomosis
*Peutz-Jeghers` Syndrome
-Autosomal dominant / Hamartoma polyp + Hyperpigmentation
-Characteristics :
.hamartomas (not malignant) (jejunum-ileum > colon > stomach)
+Associated cancer risk for women with peutz-jeghers is (Ovarian cancer)
-Other Signs :
.melanotic pigmentation (Hyperpigmentation) (black/brown) of buccal mucosa (mouth), lips, digits, palms, feet (soles), nippels
-Treatment :
.removal pf polyps
+Juvenile Polyps is (benign hamartomas in the small bowel and colon; not premalignant)
+Turcot Syndrome (Colonic polyp + CNS tumor) +Juvenile Polyp (Hemartoma / Benign)
+Colonic Volvulus (Twisting of colon on itself about its mesentery, resulting in obstruction and if complete, vascular
compromise with potential necrosis, perforation, or both / Most type of colonic volvulus is - Sigmoid volvulus)
-Condition in which diverticula can be found within the colon, especially the sigmoid; diverticula are actually false diverticula /
diverticula involve all layers of the bowel wall and RARE in the colon (False Diverticulum)
+Most common site is (Sigmoid)
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*Diverticulitis
-Infection or perforation of a diverticulum
-Pathophysiology is (obstruction of diverticulum by a fecalith)
-Symptoms :
.LLQ pain
.fever
-Diagnosis :
.Best test is (abdominal CT-scan) (colonoscopy + barium enema is contraindicated) / Best test for diverticulosis is (Colonscopy)
-Treatment :
.I.V antibiotics
.surgery (after 2 attacks / abscess or perforation)
-How common is massive lower GI bleeding with diverticulitis ?
.very RARE ! Massive lower GI bleeding is seen with diverticulosis, NOT with diverticulitis
+M.C.C of massive lower GI bleedign in adults is (Diverticulosis / 2nd cause is vascular ectasia or angiodysplasia)
+M.C.C of massive bleeding lower GI bleeding in children is (meckel's diverticulum)
+M.C.C of bleeding lower GI bleeding in children is (anal fissure)
*Hemorrhoids
-Engorgement of the venous plexuses of the rectum, anus, or both; with protrusion of the mucosa, anal margin, or both
+Internal hemorrhoid is (M.C) (hemorrhoid above the ‘proximal’ dentate line / not painful / may bleed)
+M.C.C of LGIB in young adults
+External hemorrhoid is (hemorrhoid below the dentate or pectinate line / painful / prone to thrombosis)
-Signs & Symptoms :
.anal mass / prolapse
.bleeding-per rectum (M.C symptom of internal hemorrhoids is bright red blood)
.itching
.pain (external hemorrhoids are painful)
-Causes Of Hemorrhoids :
.constipation / straining
.portal hypertension
.pregnancy
-Hemorrhoid Quadrants :
.left lateral (3 o'clock)
.right posterior (7 o'clock)
.right anterior (11 o'clock)
.circum firential (3-7-11 o'clock)
-Classification By Degree (for internal hemorrhoids) :
.1st degree hemorrhoid (NO prolapse)
nd
.2 degree hemorrhoid (prolapses with defecation, but spontaneously reduce)
.3rd degree hemorrhoid (prolapses with defecation and must be manually reduced)
41
th
.4 degree hemorrhoid (prolapsed hemorrhoid that cannot be reduced + pain)
-Treatment :
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.conservative treatment typically consists of increasing dietary fiber, sitz baths, laxatives
.grade 3-4 needs surgery (Hemorrhoidectomy)
+Contraindication for hemorrhoidectomy (crohn`s disease)
+Hemorrhoidectomy is the M.C.C of anal stricture (anal stenosis)
+You must be ruled out with lower GI bleeding believed to be caused by hemorrhoid (Colon cancer-colonoscopy) if Pt. >50yrs
**Jaundice
-Is usually detectable clinically when the plasma bilirubin exceeds 50mol/L (3mg/dL)
-Causes Of Elevated Serum Transaminases (ALT-AST):
+ (<100 U/L)
.chronic hepatitis (C-B)
.haemochromatosis
.fatty liver disease
+(100-300 U/L)
.alcoholic hepatitis
.autoimmune hepatitis
.wilson`s disease
+(>300U/L)
.drugs (paracetamol)
.acute viral hepatitis
.autoimmune liver disease
.ischaemic liver
.toxins
.flare of chronic hepatitis B
-Cholestatic Jaundice :
.is a condition where bile cannot flow from the liver to the duodenum
.causes of cholestatic jaundice (primary biliary cirrhosis, pregnancy, chronic right heart failure, alcohol, drugs ,cystic fibrosis,
severe bacterial infections, carcinoma, choledocholithiasis, parasitic infection, chronic pancreatitis)
.complications (jaundice, pale stools, dark urine, pruritus-malabsorption Vit ADEK, weight loss, steatorrhea ,osteomalacia,
bleeding tendency, xanthelasma and xanthomas)
**Ascites
-Is present when there is accumulation of free fluid in the peritoneal cavity. Small amount of ascites are asymptomatic, but with
large accumulations of fluid (>1L)
-Signs & Symptoms :
.abdominal distension
.”flank bulging” (bulging of the flanks in the reclining patient)
."shifting dullness" (difference in percussion note in the flanks that shifts when the patient is turned on the side)
."fluid wave" (tapping or pushing on one side will generate a wave-like effect through the fluid that can be felt in the opposite
side of the abdomen)
.portal hypertension (perhaps due to cirrhosis or fibrosis of the liver)
.leg swelling
.bruising
.gynecomastia
.hematemesis
.mental changes due to encephalopathy
.weight loss
.heart failure
.shortness of breath as well as wheezing and exercise intolerance
.distortion or eversion of the umbilicus
.hernia
.abdominal striae
.divarication of the recti and scrotal oedema
.dilated superficial abdominal veins may be seen if the ascites is due to portal hypertension
-Causes :
+"Transudate" (high SAAG)
42
**Cirrhosis
-Replacement of liver tissue by fibrosis as result of chronic liver disease
+Hepatic cirrhosis is a common disease characterised by diffuse hepatic fibrosis and nodule formation. It can occur at any age
+The M.C.C of cirrhosis are chronic viral hepatitis (B-C-D) and prolonged excessive alcohol consumption
+Cirrhosis is the M.C.C of portal hypertension and its associated complications
+The liver tissue shows fibrosis, cell necrosis, degeneration and regeneration nodules with loss of lobular and vascular
architecture
.esophageal varices
.fetor hepaticus
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.hypogonadism
.caput medusa
-Causes :
.alcohol (alcoholic liver disease – alcoholic cirrhosis has a worse prognosis than any cause)
.chronic hepatitis (B or C) (HBV – is M.C.C) / autoimmune hepatitis (F > M)
.non-alcoholic fatty liver disease
.immune (primary sclerosing, cholangitis, autoimmune liver disease)
.biliary (primary biliary cirrhosis (gold standard diagnosis is antimitochondrial antibodies with liver biopsy), secondary biliary,
cirrhosis, cystic fibrosis)
.genetic (hemochromatosis, wilson's disease, alpha-1 antitrypsin deficiency, DM, skin hyperpigmentation, pseudogout,
cardiomyopathy, iron overload)
.cryptogenic
.chronic venous outflow obstruction
.Budd-Chiari syndrome
+The Budd-Chiari syndrome is due to occlusion of the Hepatic veins
-Diagnosis :
.liver biopsy (Gold standard)
-Lab Findings :
.AST-ALT elevated (AST>ALT)
.alkaline phosphatase elevated
.albumin (levels fall)
.prolonged PT
.hyponatremia
.thrombocytopenia (low platelet)
.coagulation factor
.leukopenia and neutropenia
-Complications :
.ascites
.esophageal variceal bleeding
.hepatic encephalopathy (due to ammonium)
.spontaneous bacterial peritonitis (liver cirrhosis, ascites, E.coli due to spontaneous bacteria/treated by antibiotic ‘ceftriaxone’)
.carcinoma
.hypersplenism
*Cardiac Cirrhosis
-Due to chronic Rt. sided heart failure, which leads to liver congestion
-Causes :
.hepatotoxic drugs or toxins
.cystic fibrosis
.veno occlusive diseases
.budd-chiari syndrome
.IVC obstruction
.pericardial effusion
(this can lead to scarring fibrosis & cirrhosis) / Affecting middle age female (40-60yrs)
-Causes :
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.idiopathic
.autoimmune progressive
.destructive intrahepatic cholangitis
-Diagnosis :
.GGT (elevated gamma-glutamyl transferase) and alkaline phosphatase
.U/S & CT
.antibodies (antimitochondrial antibody)
Complications :-
- sicca syndrome ( dry mouth )
-malabsorption: osteomalacia, coagulopathy
- portal hypertension: ascites, variceal haemorrhage
-hepatocellular cancer
*Budd-Chiarri Syndrome
-Is a condition caused by occlusion of the hepatic veins that drain the liver
-Causes :
+Primary Budd–Chiari syndrome (75%): thrombosis of the hepatic vein
+Hepatic vein thrombosis is associated with the following in decreasing order of frequency :
.Polycythemia vera
.Pregnancy
.Postpartum state
.Use of oral contraceptives
.Paroxysmal nocturnal hemoglobinuria
.Hepatocellular carcinoma
.Lupus anticoagulants
+Secondary Budd–Chiari syndrome (25%): compression of the hepatic vein by an outside structure (e.g. a tumor)
.infection such as tuberculosis
.genetic tendencies include (protein C deficiency, protein S deficiency, the Factor V Leiden mutation)
.hormonal contraception
.other risk factors include the antiphospholipid syndrome, aspergillosis, Behçet's disease, dacarbazine, pregnancy and trauma
.alpha-3-antitrypsin deficiency
.hemochromatosis
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.steroids
.clonorchis sinensis
.polyvinyl chloride (PVC)
-Diagnosis :
.needle biopsy
-Treatment :
.surgical resection / liver transplant
.if not fit for surgery (intra-arterial chemotherapy / ethanol injection)
+Fibrolamellar hepatoma is the best prognosis / usually affect after young adult
+M.C site of metastasis is lung
+Tumor marker (hepatoma) is (elevated alpha-fetoprotein) (AFP, α-fetoprotein, alpha-1-fetoprotein, alpha-feto globulin)
+M.C location of abscess in the liver is (Rt. lobe > Lt. lobe)
+M.C type world wide is (amebic)
*Hepatocellular Adenoma
-Benign liver tumor / F > M (9:1) / Age 30-35yrs
-Histology (hepatocyte without bile duct)
+Associated with use of OCP
-M.C complications (rupture, bleeding)
-Treatment (small – stop OCP / large >5cm – surgical resection)
*Hepatic Hemangioma
-M.C benign liver tumor
-Complications :
.pain
.heart failure
.obstructive jaundice
.kasabach-merritt syndrome (thrombocytopenia-coagulopathy)
-Diagnosis :
.CT-scan with contrast
+Biopsy is contraindicated (risk of bleeding)
.sheep, pigs, camels, cattle, goats, horses, dogs and other animals are the host
-Diagnosis :
.serology (Echinococcus titer – antibody)
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*Hepatomegaly
-Is the condition of having an enlarged liver
-Sings & Symptoms :
.weight loss
.poor appetite
.lethargy
.jaundice
.bruising
-Causes :
1.Liver inflammation
+Viral (hepatitis, mononucleosis, cytomegalovirus CMV, herpes simplex HSV, yellow fever)
+Bacterial (pyaemic abscesses, brucellosis, typhoid, syphilis, leptospirosis)
+Protozoa (amoebic liver abscess, malaria, kala-azar)
+Helminth (schistosomiasis, hydatid cyst, fasciola)
2.Liver congestion
.inferior vena cava obstruction
.budd-chiari syndrome
.veno-occlusive disease
3.Obstructive jaundice
4.Liver cirrhosis
5.Neoplastic
.metastatic tumors
.hepatocellular carcinoma (liver)
.myeloma
.leukemia
.lymphoma
6.Blood diseases
.hemolytic anemia
.megaloblastic anemia
.sickle cell disease
.polycythaemia vera
.leukemia
.hodgin`s lymphoma
.non-hodgin`s lymphoma
7.Metabolic
.fatty liver
.wilson`s disease
.amyloidosis
.gaucher`s disease (lipoid storage disease)
.von gierke's disease (glycogen storage disease)
8.Drugs and alcohol
9.Biliary
.primary biliary cirrhosis
.primary sclerosing cholangitis
10.Others
47
.sarcoidosis
-Treatment :
+In the case of cirrhosis, prednisone and azathioprine for autoimmune hepatitis is used in treatment
+In the case of lymphoma the treatment options include single-agent (or multi-agent) chemotherapy and regional radiotherapy,
also surgery may be an option in specific situations
+Meningococcal group C conjugate vaccine
+In primary biliary cirrhosis ursodeoxycholic acid
*Liver Transplantation
-In case of irreversible progressive liver disease with no alternative therapy as
liver cirrhosis, fulminant liver failure and inborn errors of metabolism
-Contraindications :
.extra hepatobiliary sepsis
.metastatic malignancy
.sever cardio-pulmonary disease
.AIDS
.age above 70yrs
.previous abdominal surgery
.portal and superior mesenteric vein thrombosis
+Selection Of The Donor :
.matched for ABO blood group compatibility
.matched for liver size
.negative HIV-HBV-HCV
+Immunosuppression :
.cyclosporine
.prednisone
.azathioprine
-Complications :
.graft rejection
.graft dysfunction (hepatic artery thrombosis, biliary leak or obstruction, recurrence of hepatitis)
.infections
.renal dysfunction
.neuropsychiatric disorders
**Gallstone
-Presence of stones in the gallbladder is referred to as cholelithiasis
-Characteristics And Composition :
.mixed stones (M.C type)
nd
.cholesterol stones (2 M.C)
+2
.pigment stones (Ca bilirubinate) (is seen in hemolytic disease)
-Signs & Symptoms :
.may be asymptomatic (do not require treatment)
.pain in the upper Rt. Side of the abdomen (RUQ pain) radiate to Rt. shoulder or scapula
.nausea, vomiting
.a Pt. may also experience referred pain between the shoulder blades or below th Rt. Shoulder
.positive Murphys sign (on physical findings) (seen too in cholecystitis)
48
-Causes :
.female, faty, fertile (multiparity), fair, forty (40yrs of age)
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*Acute Cholecystitis
-Obstruction of cystic duct leads to inflammation of the gallbladder
-Risk factor is (Gallstones)
-Signs & Symptoms :
.unrelenting RUQ pain or tenderness
.fever
.nausea, vomiting
.painful palpable gallbladder
.positive Murphy`s sign (acute pain and inspiratory arrest elicited by palpation of the RUQ during inspiration) (negative – stones
and cholangitis)
.right subscapular pain (referred)
.epigastric discomfort (referred)
-Complications :
.abscess
.perforation
.choledocholithiasis
.cholecystoenteric fistula formation
.gallstones ileus
-Lab Results :
.increased WBS
.elevation in alkaline phosphatase
.LFTs
.elevation in amylase
-
MAOIs
halothane
anti-tuberculosis: isoniazid, rifampicin, pyrazinamide
statins
alcohol
amiodarone
methyldopa
Liver cirrhosis
methotrexate
methyldopa
amiodarone
*risk may be reduced with erythromycin stearate
The gold standard investigation of bacterial overgrowth is small bowel aspiration and culture
50Page
NEPHROLOGY
**Chronic Renal Disease CRD-CKD
-Is a progressive loss in renal function over a period of months or years
-Glomerular filtration rate (GFR) is the best overall index of kidney function
+The M.C.C of death in people with CRD is therefore cardiovascular disease rather than renal failure
+Creatinine levels may be normal in the early stages of CKD, and the condition is discovered if urinalysis, shows that is allowing
the loss of protein
-Signs & Symptoms :
.HTN (Bp is increased due to fluid overload and production of vasoactive hormones created by the kidney via the RAS ‘renin-
angiotensin system’)
.urea accumulates (leading to azotemia and ultimately uremia - symptoms ranging from lethargy to pericarditis and
encephalopathy)
."uremic frost" (is excreted in eccrine sweat at high concentrations and crystallizes on skin as the sweat evaporates)
.sweating
.hyperkalemia (potassium accumulates in the blood - hyperkalemia with a range of symptoms including malaise and potentially
fatal cardiac arrhythmias)
+Hyperkalemia usually does not develop until the glomerular filtration rate falls to less than 20-25 ml/min/1.73 m 2
+Hyperkalemia in CKD can be exacerbated by acidemia (which leads to extracellular shift of potassium) and from lack of insulin
.erythropoietin synthesis is decreased causing anemia
.fluid volume overload (symptoms may range from mild edema to life-threatening pulmonary edema)
.hyperphosphatemia (due to reduced phosphate excretion) follows the decrease in glomerular filtration
+Hyperphosphatemia is associated with increased cardiovascular risk
.hypocalcemia, due to 1,25 dihydroxyvitamin D3 deficiency (caused by stimulation of FGF-23 and reduction of renal mass)
+Later, this progresses to secondary hyperparathyroidism, renal osteodystrophy (brown tumor of bone), and vascular
calcification that further impaired cardiac function
.metabolic acidosis
.sexual dysfunction is very common in both men and women with CKD
+A majority of women have trouble with sexual arousal, and painful menstruation
-Causes :
.DM (M.C.C)
.HTN
.glomerulonephritis
.polycystic kidney disease
.drug and toxin induced chronic tubulointerstitial nephritis
.obstructive nephropathy (kidney stones, diseases of prostate)
.recurrent pyelonephritis (M.C bacteria is E.coli)
.SLE
.vascular diseases (bilateral renal artery stenosis)
.amyloidosis
51
2
.stage 1 (slightly diminished function; kidney damage with normal or relatively high GFR >90mL/min/173m )
.stage 2 (mild reduction in GFR 60-90mL/min/173m2)
2
.stage 3 (moderate reduction in GFR 30-59 mL/min/173m )
2
.stage 4 (15-30mL/min/173m )
.stage 5 (end stage renal disease ESRD <15) (treated by dialysis, renal transplant BEST)
-Treatment :
.control of Bp and treatment of the original disease ‘DM’
.replacement of erythropoietin and calcitriol-‘Vit D3’
.phosphate binder (used to control the serum phosphate levels)
.when one reaches stage 5 CRD, renal replacement therapy, dialysis, transplant (BEST)
+Drugs are contraindicated in chronic renal failure :
.Tetracycline
.Nalidixic acid
.Nitrofurantoin
.Aspirin
+In chronic renal failure the serum concentration of the following substances is increased :
.Uric acid
.Urea
.Creatinine
.Phosphorus
+Glomerular filtration rate GFR = creatinine clearance’ (normal is 100-140ml/min)
(140-age) * Mass (in Kg) * 0.85 (if female)
72 * creatinin
+GFR (age, mass, creatinine, sex) / Low GFR (renal failure) / High GFR (pregnancy, early DM)
++Urine Retention
+Acute (painful / prostatic hyperplasia is M.C.C / bladder capacity is normal 700-1000cc / rapid foley's)
+Chronic (painless / prostatic hyperplasia is M.C.C / bladder capacity up to 4L / NOT rapid)
.glomeruli
.renal tubules
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.interstitium
.rhabdomyolysis
.tumor lysis syndrome
+Post-renal (urinary tract obstruction, benign prostatic hyperplasia, kidney stones) (urea creatinine <20:1 / urine <350 / FENa
>1%)
.urinary tract obstruction
.benign prostatic hyperplasia
.kidney stones
.obstructed urinary catheter
.bladder stone
.bladder, ureteral or renal malignancy
+Other causes :
.Goodpasture’s syndrome
.Hemolytic uremic syndrome
.Scleroderma crisis
.Post infectious glomerulonephritis
.Severe dehydration
.Severe burn
.Severe hemorrhage
.Hemolytic uremic syndrome
-Complications :
.metabolic acidosis
.hyperkalemia
.hypocalcemia
.hypoalbuminemia
.hyperphosphatemia
.pulmonary edema
.bleeding (inhibit platelet)
.pericarditis
+Retrosternal chest pain – cough (increased in lying supine) (decreased in leaning forward) (Diffuse ST-elevation)
-Diagnostic test :
.the blood urea nitrogen BUN
+A diagnosis is made when there is rapid reduction in kidney function, as measured by serum creatinine, or based on a rapid
reduction in urine output, termed oliguria (less than 400 mls of urine per 24 hours)
-Treatment :
.in pre renal ARF, administration of IV fluid (is 1st step)
.NSAIDs (ibuprofen, iodinated contrast)
.antibiotics (gentamicin)
+Indications of dialysis in ARF :
.refractory HTN or pulmonary edema
.uncontrollable hyperkalemia >7
.uremic encephalitis
.pericarditis
.bleeding diathesis (epistaxis, GI bleeding)
.severe metabolic acidosis Ph<7
.blood urea nitrogen BUN >70-100 mg/dl
+Pre-renal (urea >20:1 / urine >500 / FENA <1%)
+Renal or Post-renal (urea <20:1 / urine <350 / FENA >1%)
**Azotemia
-Is a medical condition characterized by abnormally high levels of nitrogen-containing compounds (such as urea, creatinine,
various body waste compounds, and other nitrogen-rich compounds) in the blood. It is largely related to insufficient or
dysfunctional filtering of blood by the kidneys. It can lead to anemia if not controlled
+Is a form of renal insufficiency caused by diminished perfusion of the kidney on`any basis. The kidney itself is normal - is an
abnormally high level of nitrogen waste products in the blood
-Signs & Symptoms :
53
*Prerenal Azotemia
-Prerenal azotemia is caused by a decrease in blood flow (hypoperfusion) to the kidneys. However, there is no inherent kidney
disease
-It Can Occur Following :
.hemorrhage
.shock
.volume depletion
.congestive heart failure
.adrenal insufficiency
.narrowing of the renal artery among other things
+The BUN : Cr in prerenal azotemia is greater than 20
*Postrenal Azotemia
-Blockage of urine flow in an area below the kidneys results in postrenal azotemia / From bilateral obstruction to the flow of
urine out of the kidney. Like in prerenal azotemia, there is no inherent renal disease / The increased resistance to urine flow can
cause back up into the kidneys, leading to hydronephrosis
+You cannot get renal failure by the obstruction of only a single kidney if a Pt. has both kidneys in place (only one kidney does
not cause renal failure – creatinine will only begin to rise when you have lost at least 70-80% of renal function)
+Acute tubular necrosis ATN is the most common cause of ARF (intrinsic) in hospitalized Pts.
-Causes :
.congenital abnormalities (vesicoureteral reflux)
.blockage of the ureters by kidney stones
.pregnancy
.compression of the ureters (by cancer, prostatic hyperplasia, or blockage of the urethra by kidney)
.bladder stones
.bilateral ureteral disease (retroperitoneal fibrosis)
.neurogenic bladder (or any other cause of bilateral obstructive disease)
+large stone in one ureter cannot cause renal failure because the creatinine does not rise if there is a loss of only one kidney. A
small tone or clot in the bladder can obstruct both kidneys and this can cause post renal azotemia
+The BUN:Cr in postrenal azotemia is initially >1
.kidney failure
.jaundice
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*Tubulointerstitial Disease
1.Acute Tubular Necrosis ATN
-Is a medical condition involving the death of tubular epithelial cells that form the renal tubules of the kidneys
-The presence of "muddy brown casts - a type of granular cast” of epithelial cells found in urinalysis is pathognomonic for ATN /
high urine sodium >40 and low urine osmolality <350
-ATN presents with acute kidney failure-injury (AKI) and is one of the M.C.C of AKI. Common causes of ATN include low blood
pressure and use of nephrotoxic drugs
-ATN may be classified as either toxic or ischemic :
.Toxic ATN occurs when the tubular cells are exposed to a toxic substance (nephrotoxic ATN)
.Ischemic ATN occurs when the tubular cells do not get enough oxygen, a condition that they are highly sensitive and
susceptible to, due to their very high metabolism
-Phases :
.Prodromal - this is time between the acute injury and the onset of renal failure
.Oliguric - <400mL per 24hrs or Anuric-<100mL per 24hrs
56
.Postoliguric - this is a diuretic phase when all the water not previously excreted will now leave the body in a vigorous polyuria
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**Glomerulonephritis GN
-Several kidney diseases (usually affecting both kidneys). Many of the diseases are characterised by inflammation either of the
glomeruli or of the small blood vessels in the kidneys, hence the name, but not all diseases necessarily have an inflammatory
component / Autoimmune event, circulating antibodies or vasculitis
+RBCs cast urinary findings is most characteristic of glomerulonephritis / Erythrocyte casts is most characteristic of acute
glomerulonephritis
-As it is NOT strictly a single disease, its presentation depends on the specific disease entity: it may present with :
.hematuria and/or proteinuria (blood or protein in the urine)
.or as a nephrotic syndrome, a nephritic syndrome, acute kidney injury, or chronic kidney disease
-DM and HTN cause glomerular disease and are certainly the most common causes of nephrotic syndrome and end-stage renal
disease
-All Forms Of GN Can Be Characterized By :
.edema (can found anywhere)
.hematuria
.red cells casts
.HTN
.low urine sodium with a fractional excretion of sodium of <1%
-Causes Of GN :
1.Vascular Disease
.wegener granulomatosis
.churg-strauss syndrome
.henoch-schonlein purpura
.polyarteritis nodosa
.TTP
.hemolytic uremic syndrome HUS
.cryoglobulinemia
2.Glomerular Disease
57
.goodpasture syndrome
.post infectious glomerulonephritis
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**Nephritic Syndrome
-Is a collection of signs (known as a syndrome) associated with disorders affecting the kidneys, more specifically glomerular
disorders
-Signs & Symptoms :
.hematuria (blood in the urine) - with RBC casts present in the urine
.proteinuria (protein in the urine) – small amounts of protein (<3.5g/day or <40mg/day)
.hypertension (high Bp – mild)
.blurred vision
.azotemia (elevated blood nitrogen)
.oliguria (low urine output <400ml/day)
-Causes :
+Nephritic syndrome is caused by inflammation of glomerulus and has urine waste, furthermore the cause can be infectious,
autoimmune or thrombotic
+Children/Adolescents
.IgA nephropathy (berger`s disease - M.C.C of GN in adult)
.Post-streptococcal glomerulonephritis (common in children)
.Hemolytic uremic syndrome HUS (M.C.C od acute renal failure in children)
.Henoch-Schonlein purpura
+Adults
.Goodpasture syndrome (hemoptysis + hematuria)
.hepatitis B-C
.Infective endocarditis
.membranoproliferative GN1
.membranoproliferative GN2
.Rapidly progressive glomerulonephritis (RPGNs)
.PTT
.SLE or lupus nephritis (worse type)
.vasculitis
+Myeloma is most prominently a cause of nephritic syndrome
-Diagnosis :
+The classic diagnosis of nephritic syndrome is post-streptococcal glomerulonephritis, which is a common complication of
Streptococcus bacterial infections, typically of the skin.
+Tests done to diagnose if an individual has nephritic syndrome are :
.blood electrolytes
.blood urea nitrogen
.potassium test
.protein in the urine
.urinalysis
.kidney biopsy
+The difference between the basis of allergic interstitial nephritis and direct toxins is that allergic nephritis occurs with the first
dose and is associated with fever, rash, joint pain and eosinophils in both blood and urine
*Goodpasture Disease
-Is a rare autoimmune disease in which antibodies attack the basement membrane in lungs and kidneys, leading to bleeding
from the lungs and kidney failure (Goodpasture syndrome may quickly result in permanent lung and kidney damage, often
leading to death). It is thought to attack the alpha-3 subunit of type IV collagen, which has therefore been referred to as
Goodpasture's antigen
+The anti glomerular basement membrane (GBM) antibodies primarily attack the kidneys and lungs / Hemoptysis + Hematuria
-Signs & Symptoms :
59
.malaise
.weight loss
Page
.fatigue
.fever
.chills
.joint aches and pains
.lung symptoms usually antedate kidney symptoms
+Lung symptoms, include (coughing up blood, chest pain (in less than 50% of cases overall), cough, and shortness of breath)
+Kidney symptoms, include (blood in the urine, protein in the urine, unexplained swelling of limbs or face, high amounts of urea
in the blood, and high blood pressure)
-Causes :
.exposure to organic solvents (e.g. chloroform) or hydrocarbons
.exposure to tobacco smoke
.certain gene mutations (HLA-DR15)
.infection, such as influenza A
.cocaine inhalation
.metal dust inhalation
.bacteraemia
.sepsis
.high-oxygen environments
.treatment with antilymphocytic treatment (especially monoclonal antibodies)
progression
+HUS
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.hemolytic anemia
.thrombocytopenia
.fever
.renal failure
.don't cause neurological symptoms
+Usually occur post-infection by E.coli 157:H7 (and causes bloody diarrhea)
+Don't give antibiotic for bloody diarrhea (increased risk of HUS) and don't transfuse platelets
**Nephrotic Syndrome
-Is a nonspecific kidney disorder characterized by three signs of disease (large proteinuria, hypoalbuminemia, and edema)
+Essentially, loss of protein through the kidneys (proteinuria) leads to low protein levels in the blood (hypoalbuminemia), which
causes water to be drawn into soft tissues (edema)
+Very low hypoalbuminemia can also cause a variety of secondary problems, such as water in the abdominal cavity (ascites),
61
around the heart or lung (pericardial effusion, pleural effusion), high cholesterol (hence hyperlipidemia), loss of molecules
regulating coagulation (hence increased risk of thrombosis)
Page
.preeclampsia
.Sarcoidosis
Page
.Syphilis (kidney damage can occur during the secondary stage of this disease - between 2 and 8 weeks from onset)
.Sjögren's syndrome (this autoimmune disease causes the deposit of immune complexes in the glomeruli, causing them to
become inflamed, this is the same mechanism as occurs in systemic lupus erythematosus)
.HIV
.Multiple myeloma
.Vasculitis
.Cancer
.Genetic disorders (congenital nephrotic syndrome is a rare genetic disorder in which the protein nephrin)
.Drugs ( e.g. gold salts, penicillin, captopril)
-Diagnosis :
.24hrs urine protein measurment (Best test)
.hypoalbuminemia (<2.5g/dL)
.high levels of cholesterol (hypercholesterolemia, elevated LDH)
-Complications :
.venous thrombosis
.infection
.hypothyroidism
.hypocalcemia
.Vit D deficiency
.microcytic hypochromic anemia
-Treatment :
.immunossuppresion for the glomerulonephritides (corticosteroids, ciclosporin)
+Nephritic syndrome
(proteinuria <3.5 gm/day - <40mg/day) (hematuria, HTN, renal failure, mild edem)
+Nephrotic syndrome
(proteinuria >3.5gm/day - >40gm/day) (sever edema – mainly face and more in morning, NO hematuria, NO HTN)
.Diabetes mellitus
.Sarcoidosis
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*Amyloidosis
-Is a rare disease that results from the buildup of misfolded proteins known as amyloids. They become insoluble and deposit in
organs or tissues, disrupting normal function
+Amyloid deposition in the kidneys can cause nephrotic syndrome, which results from a reduction in the kidney's ability to filter
and hold on to proteins. The nephrotic syndrome occurs with or without elevations in creatinine and blood urea concentration
-Signs & Symptoms :
.deposition of amyloids in the liver can lead to elevations in serum aminotransferases and alkaline phosphatase
.liver enlargement is common. Spleen enlargement is rare
.presence of Howell-Jolly bodies on blood smear
.malabsorption
.enlarged tongue
.obstructive sleep apnea
.difficulty swallowing
.thyroid and adrenal gland can be infiltrated
.hypothyroidism
.orthostatic hypotension (low blood sodium concentration may be attributed to autonomic neuropathy and heart failure)
+Amyloid deposits occur in the pancreas of Pts. with diabetes mellitus
-Types :
1.AL (plasma cell dyscrasia causing deposition of protein derived from immunoglobulin light chains. This may be associated with
multiple myeloma)
2.AA (amyloid is produced as a proteinaceous material in association with multiple chronic infectoius or inflammatory
conditions, such as rheumatoid arthritis, inflammatory bowel disease or myeloma)
-The amyloid protein builds up in the (associated with) :
.kidney (causing glomerulonephritis)
.GI tract (malabsorption)
.nerves
.muscles
.heart (amyloid associated with restrictive cardiomyopathy, rhythm disorders and heart block)
.macroglossia
.neural involvement produces carpal tunnel syndrome
-Diagnosis :
.congo red testing shows green birrefringence
-Treatment :
.melphalan and prednisone can control protein production
*Alport Syndrome
-Is a genetic disorder affecting children, characterized by glomerulonephritis, end-stage kidney disease, and hearing loss. Alport
syndrome can also affect the eyes, though the changes do not usually affect sight, except when changes to the lens occur in
later life
+Hereditary nephritis (X-linked dominant); renal biopsy shows foam cells (Genetic family history)
-Signs & symptoms :
.hematuria
.proteinuria
.hearing loss (hearing is normal at birth. Hearing loss develops progressively, usually at the stage when kidney function is
normal)
.eye changes (abnormalities are often be seen including lenticonus, keratoconus, cataracts as well as retinal flecks in the macula
and mid-periphery. Severe cases may require a corneal transplant)
.aortic dissection
.leiomyomas (tumours of smooth muscle affecting the oesophagus and female genital tract, may occur in a rare overlap
syndrome involving the adjacent COL4A5 and COL4A6 genes)
64
**Metabolic Acidosis
-Anion Gap = (Na+ + K+) – (CL- + Hco-3) or Na+ – (CL + Hco-3) (normally, this concentration is about 8-16 mmoL)
Page
-Causes :
1.increased anion gap, causes including :
.lactic acidosis
.DKA
.CRF
.intoxication (ethanol, salicylates, methanol, formaldehyde, INH, paraldehyde, sulfates, metformin-glucophage)
.massive rhabdomyolysis
2.normal angion gap, causes including :
.long standing diarrhea (bicarbonate loss)
.pancreatic fistula
.ureterosigmoidostomy
.renal tubular acidosis RTA
+Causes Of Metabolic Acidosis With Anion Gap :
.Renal failure
.Diabetic ketoacidosis
.Lactic acidosis
.Aspirin overdose
.Alcohol poisoning
.Uremia
.Salicylate poisoning
.Metformin
.Insulin deficiency
.Diarrhea
.Shock states and cardiac arrest
.Small intestinal fistula
.Ulcerative colitis
.Ureteroenterostomy
.Renal insufficiency
.Carbon monoxide poisoning
.Biliary fistula
.Hemorrhagic shock
.Starvation
.Renal failure
.Small bowel fistula
.Diabetes mellitus
.Severe dehydration
.Renal insufficiency
.Renal Fanconi syndrome
**Metabolic Alkalosis
-Causes :
.vomiting (alkalosis) / +Diarrhea (acidosis)
.diuretics therapy (thiazides – loop diuretics)
.hyperaldosteronism (conn's syndrome)
**Respiratory Acidosis
-Hypoventilation (increased Co2)
-Causes :
.increased blood carbon dioxide concentration
.decreased pH (a condition generally called acidosis)
**Respiratory Alkalosis
-Hyperventilation (decreased Co2)
+Medical condition in which increased respiratory elevated the bloob pH
65
.pH (7.35-7.45)
.Hco3-Bicarbonate (16-24) (kidney-alkalosis)
.Co2 (35-40) (respiratory-acidosis)
**Hypertension
-Bp (120/80)
-Pre HTN (systolic 120-139 / diastolic 80-89)
-Hypertension (stage 1 – systolic 140-159 / diastolic 90-99) (stage 2 – systolic >160 / diastolic >100)
-Laboratory Investigation :
.urinalysis for protein, glucose and red blood cells
.hematocrit
.serum potassium to exclude hyperaldosteronism
.serum creatinine and BUN
.electrocardiogram to evaluate for left ventricular hypertrophy
.glucose and plasma lipid analysis as an indicator of atherosclerotic risk
-Indications for specific hypertensive groups :
.diabetics (should be treated with ACE inhibitors or ARBs, which prevent the development of nephropathy / The blood pressure
goal in a diabetic is lower, at <130/80 mmHg, this is also true in those with renal insufficiency, CHF, retinopathy or stroke and
Pts. with macroalbuminuria should receive an ACE inhibitor)
.post myocardial infarction (ischemic heart disease) (should be treated with beta blockers), diminished left-ventricular systolic
function (such as congestive heart failure and postMI, should receive ACE inhibitors and/or ACE inhibitors)
.pregnant Pts. are best treated with alpha-methyldopa, labetalol, hydralazine or calcium-channel blockers (ACE inhibitors and
angiotensin-receptor blockers are absolutely contraindication in pregnant Pts. Diuretics are relatively contraindicated)
-Causes of secondary hypertension :
.renal artery stenosis (M.C.C)
.cushing syndrome
.renal disease
.vascular disease
.pheochromocytoma
.conn's syndrome (primary hyperaldosteronism)
-Who should be screened for secondary hypertension ?
.those who become hypertensive either very young or very old (<25->55)
.those with a key feature of history
.Pts. who remain hypertensive despite increasing doses and numbers of anti-hypertensive medications
*Diuretics
-Specific Indications :
.CHF
.edematous states
.african-american Pts.
-Side Effects :
.decreases in potassium and magnesium
.increases in calcium
.uric acid
.glucose
.LDL-cholesterol
.gynecomastia
-Relative contraindications :
.diabetes
.gout
.hyperlipidemia
*Beta-Blockers
+Metoprolol and atenolol are the most commonly used
-Specific Indications :
.MI
66
**Polyuria
-Polyuria is a condition usually defined as excessive or abnormally large production or passage of urine (greater than 2.5 or 3 L
over 24 hours in adults)
-Causes :
.General (polydipsia, psychogenic polydipsia, diuretic drugs, osmotic diuresis)
.Urinary system (interstitial cystitis, urinary tract infection, renal tubular acidosis, fanconi syndrome, nephronophthisis-genetic)
.Hormonal (hypokalemia, DM, use of a corticosteroid, pheochromocytoma, hyperparathyroidism, Diabetes insipidus,
hypercalcaemia, hyperthyroidism, hypopituitarism, Conn's disease, hyperglycemia)
.Circulation (congestive heart failure, Cardiorespiratory disease, postural orthostatic tachycardia syndrome POTS)
.Neurologic (cerebral salt-wasting syndrome, neurologic damage, migraine)
.Other (high doses of riboflavin (vitamin B2), high doses of vitamin D, altitude diuresis, side effect of lithium, Hemochromatosis)
+Polyuria and polydipsia can be due to :
.Deficiency of arginine and vasopressin
.Deficiency of insulin
.Hypercalcemia
.Psychogenic causes
67
**Hematuria
Page
-Is the presence of red blood cells (erythrocytes) in the urine. It may be idiopathic and/or benign, or it can be a sign that there is
a kidney stone or a tumor in the urinary tract (kidneys, ureters, urinary bladder, prostate, and urethra), ranging from trivial to
lethal. If white blood cells are found in addition to red blood cells, then it is a signal of urinary tract infection
+Painless hematuria is the leading presentation of Renal cell carcinoma
-Types :
1.Red blood cells
.Microscopic hematuria (small amounts of blood, can be seen only on urinalysis or light microscopy)
.Macroscopic hematuria (or "frank" or "gross" hematuria)
2.Hemoglobin (only the red pigment, not the red blood cells)
3.Other pigments
.Myoglobin in myoglobinuria
.Porphyrins in porphyria
.Betanin, after eating beets
.Drugs (rifampicin, phenazopyridine and sulphonamides)
-Causes :
.UTI (Escherichia coli)
.nephrolithiasis (stones in the kidney, bladder or ureter)
.polycystic kidney disease
.trauma
.cancer of the kidney, prostate or bladder
.benign prostatic hyperplasia, in older men, especially those over 50
.vigorous exercise
.glomerular bleeding (IgA nephropathy ("Berger's disease"), Alport syndrome, thin basement membrane disease)
.sickle cell disease
.schistosomiasis (caused by Schistosoma haematobium)
.recent instrumentation of the urinary tract
.prostatitis
.urethritis
.kidney diseases
.arteriovenous malformation of the kidney
.renal tuberculosis
.malignant hypertension (fibrinoid necrosis)
.cystitis
.prostate carcinoma
.tuberculosis
.papillary necrosis, renal cysts, renal calculus
.allergy (rarely cause episodic gross hematuria in children)
.left renal vein hypertension, also called "nutcracker phenomenon" or "nutcracker syndrome"
.march hematuria (secondary to repetitive impacts on the body, usually the feet)
.athletic nephritis (secondary to strenuous exercise)
.alport syndrome
.Infective endocarditis
.medications can cause red discoloration of the urine, but not hematuria. Some examples include (sulfonamides, quinine,
rifampin, phenytoin, use of anticoagulants)
.consumption of beets ("beeturia")
.menstruation
**Proteinuria
-The presence of an excess of serum proteins in the urine. The excess protein in the urine often causes the urine to become
foamy, although foamy urine may also be caused by bilirubin in the urine (bilirubinuria), retrograde ejaculation, pneumaturia
(air bubbles in the urine) due to a fistula, or drugs such as pyridium
-Causes :
.people with diabetes (M.C.C) (may have damaged nephrons and develop proteinuria) - Diabetic nephropathy (M.C.C)
.due to disease in the glomerulus (membranous glomerulonephritis)
.because of increased quantity of proteins in serum (overflow proteinuria)
68
.Waldenstrom's macroglobulinemia
.Chronic lymphocytic leukemia
Page
.Amyloidosis
.Malignancies (e.g., lymphoma, other cancers)
.Multiple myeloma
.Monoclonal Gammopathy of Renal Significance
+Bence Jones protein is a monoclonal globulin protein or immunoglobulin light chain found in the urine
+Proteinuria secondary to autoimmune disease should be treated with steroids or steroid-sparing agent plus the use of ACE
inhibitors
.Na+ Hco3
Page
*Type-4 RTA
-Can Causes :
.hyperkalemia
.aldosterone deficiency (hypoaldosteronism) (Primary vs. hyporeninemic)
.aldosterone resistance (Drugs - NSAIDs, ACE inhibitors and ARBs, Eplerenone, Spironolactone, Trimethoprim, Pentamidine)
.pseudohypoaldosteronism
**Dialysis
-Types :
Hemodialysis
Peritoneal dialysis (easier to perform - simple, done at home)
-Substances :
.Ethylene glycol .Procainamide .Methanol .Isopropyl alcohol .Barbiturates .Lithium
.Bromide .Sotalol .Chloral hydrate .Ethanol .Acetone, Atenolol .Theophylline .Salicylates
-Complications :
.cardiovascular disease (M.C.C of death)
.anemia (low erythropoietin)
.protein loss
.bleeding (heparin)
+2
.renal osteodystrophy and osteitis fibrosa cystica (secondary hyperparathyroidism) (low Ca and lead to elevated PTH)
+Renal osteodystrophy is a bone disease that occurs when your kidneys fail to maintain proper levels of calcium and
phosphorus in the blood. It's common in people with kidney disease and affects most dialysis patients
.infection (HBV, HCV)
.amyloidosis
.renal cyst (acquired renal cyst)
.renal cancer (increased risk of renal cancer)
.urinate frequently (or an urge to urinate) in the absence of vaginal discharge and significant pain
.foul smelling urine are presenting complaints
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**Hypernatremia
-Is an elevated sodium level in the blood
-Signs & Symptoms :
.coma
.signs of dehydration (dry skin, confusion, oliguria, dry mucous membranes, tachycardia, orthostatic hypotension, seizures)
.increased (albumin, urea)
.lethargy
.edema
.delirium
.come
-Causes :
.fluid loss (diarrhea, vomiting, burns)
.incorrect IV fluid replacement (excessive saline)
.diabetes insipidus
.head injury
.CNS surgery
.osmotic diuresis (diabetic coma)
.primary aldosteronism
.Conn's syndrome
+Hypovolemic hypernatremia (dehydration, diarrhea, vomiting)
+Euvolemic hypernatremia (diabetes insipidus)
+Hypervolemic hypernatremia (Conn's syndrome-primary aldosteronism)
**Hypokalemia
+ +
-Hypopotassemia (ICD-9), refers to the condition in which the concentration of potassium (K ) in the blood is low (if K
<2.5mmol/L) (K+ major intracellular) (Na+ major extracellular)
-Signs & Symptoms :
.elevation of blood pressure (hypotonia)
.abnormal heart rhythm
.muscle weakness
.myalgia, tremor
.muscle cramps
.constipation
.hyporeflexia
.rhabdomyolysis
.respiratory depression
.sluggish or absent intestinal movements
.ECG (inverted T waves, U wave, ST depression, and a wide PR interval)
-Causes :
.diuretics (thiazide, furosemide)
.vomiting
.diarrhea
.hypomagnesemia
.alkalosis
.pyloric stenosis
.villous adenoma rectum
.intestinal fistula
.cushing`s syndrome
.steroids-lasix / ACTH
.conn`s syndrome (primary hyperaldosteronism)
.cushing syndrome
.renal tubular failure
.renal tubular acidosis
.periodic paralysis
75
.Bartter's syndrome
.Ileostomy
Page
**Hyperkalemia
-Signs & Symptoms :
.plasma potassium >6.5mmol/L
.malaise
.palpitations
.muscle weakness
.metabolic acidosis
.cardiac arrhythmia
.sudden cardiac death
.ECG (Peak T wave, Wide QRS, Prolonged PR, Ventricular Fibrillation)
-Causes :
.oliguric renal failure (acute and chronic)
.glomerulonephritis
.hemolysis
.K+ sparing diuretics
.rhabdomyolysis
.burn
.matabolic acidosis
+
.excess K therapy
.addison`s disease
.massive blood transfusion
.drugs (ACE-suxamethonium-captopril) (corticosterois are not cause of hyperkalemia)
-Treatment :
.Calcium resonium
.Salbutamol
.IV calcium gluconate
.IV glucose and insulin
.IV furosemide
.IV sodium bicarbonate
**Hypocalcemia
-Normal blood calcium level is between 8.5 to 10.5 mg/dL (2.12 to 2.62 mmol/L)
-Signs & Symptoms :
.Petechiae which appear as on-off spots
.purpura
.depression
.oral, perioral and acral paresthesias
.tetany
76
.chvostek's sign
.trousseau's sign
Page
.laryngo-spasm
.cardiac arrhythmias
.ventricular tachycardia
.ECG (QT prolongation - prolonged S-T interval)
.numbness and circumoral tingling
.carpopedal spasm
.abdominal cramps
-Causes :
.thyroid or parathyroid surgery (thyroidectomy)
.parathyroid hormone PTH deficiency
.Vit D deficiency (decreased sun exposure)
.hypoparathyroidism
.pancreatitis
.over-hydration
.respiratory alkalosis
.celiac disease
.intestinal malabsorption
.medullary thyroid cancer (increased calcitation – Ca+2)
.blood transfusion
.magnesium deficiency
.exogenous inorganic phosphate excess
.DiGeorge syndrome
.renal failure (acute or chronic)
+Side effects of furosemide :
.Hypokalemia
.Hyperuricemia
.Hyperglycemia
.Ototoxicity
**Hypercalcemia
-Signs & Symptoms :
.stones (renal or biliary)
.bones (bone pain)
.groans (abdominal pain, nausea and vomiting)
.thrones (polyuria - also looks like osborn wave on ECG)
.psychiatric overtones (depression, anxiety, cognitive dysfunction, insomnia, coma)
.ECG (short QT interval)
.peptic ulcers
.cardiac arrest
.constipation
.abdominal pain
.vomiting
.weigh loss
.polydipsia
.polyuria
.HTN
.weakness and confusion
-Causes :
.malignancy (myeloma, bone metastases, lung cancer)
.hyperparathyroidism
.Vit D intoxication (hypervitaminosis D)
.sarcoidosis
.milk-alkali syndrome
.addison's disease
.thyrotoxicosis
.thiazide use
77
-Treatment :
.diuretics (furosemide)
.steroids
Page
.bisphosphonates
.salmon calcitonium
.chemotherapy (for malignancy)
+Tetany may occur in :
.Hyperventilation syndrome
.Metabolic alkalosis
.Hypocalcemia
.Hypomagnesaemia
+The serum alkaline phosphatase level is characteristically normal in Hemolytic Jaundice
+Causes of hyperuricemia :
.High dose aspirin
.Chronic renal disease
.Alcohol
.Leukemia
.Carcinoma
.Severe psoriasis
+Causes of osteoporosis :
.Acromegaly
.Corticosteroids
.Lack of exercise
.Smoking
+Recommended treatment for osteoporosis includes :
.Estrogen
.Exercise
.Calcium
.Vit D
+Renin is secreted by Juxtaglomerular apparatus
**Hyperglycemia
-Causes :
.steroid (cortisone)
.anti-HiV medication / anti-TB drugs
.thiazide
.pancreatic problems (pancreatitis, pancreatic surgery, pancreatic cancer)
.cushing disease
.acromegaly
.pheochromocytoma
.hyperthyroidism
.pregnancy
.metabolic syndrome (Syndrome X)
.obesity
.HTN
.hyperlipidemia
.asian
.renal failure
.PCOs
.cystic fibrosis
**Hypoglycemia
-Causes :
.exogenous insulin (DM Pt. who take overdose of insulin or missed meal) (munchausen syndrome)
.panhypopituitarism
.liver failure or severe hepatitis
.addison disease (adrenal insufficiency)
.insulinoma or nesidioblastosis (diffuse B-cell hyperplasia)
78
.alcoholism
.dumping syndrome (post-prandial hypoglycemia)
+Treatment (25-50mL glucose I.V) (IM glucagon – short action and repeat after 20mins)
Page
+Neuro-muscular
.Myoclonus
.Hyporeflexia
.Ataxia
.Pathological reflexes
.Tremor
.Asterixis
+Respiratory
.Cheyne-Stokes respiration
+Neurological
.Dysarthria
.Lethargy
.Confusion
.Delirium
.Seizures
.Coma (from cerebral edema)
-Causes :
.infections (Meningitis, Encephalitis, brain abscess, rocky mountain spotted fever, AIDS)
.trauma, Subarachnoid hemorrhage, subdural hematoma, cavernous sinus thrombosis
.hydrocephalus
.Guillain-Barré syndrome
.multiple sclerosis
.cancers (carcinomas, lung cancers ‘small-cell lung cancer, mesothelioma’, GI cancers ‘stomach, duodenum, pancreas’,
genitourinary cancers, bladder, urethral, prostate, endometrial’)
.lymphoma
.sarcomas (Ewing's sarcoma)
.pulmonary causes (pneumonia, lung abscess)
.asthma
.cystic fibrosis
.transient causes (endurance exercise, general anesthesia)
.hereditary causes
.sarcoidosis
+Drugs can cause SIADH :
.Chlorpropamide
.Ciprofloxacin
.Clofibrate
.Moxifloxacin
.Phenothiazine
.Ifosfamide
.Cyclophosphamide
.Carbamazepine
79
.Oxcarbazepine
.Valproic Acid
Page
.surgery (if medical therapy cannot be tolerated or if it fails to reduce prolactin levels)
*Hyperprolactinemia
-Is the presence of abnormally high levels of prolactin in the blood
+Normal levels are less than 500 mIU/L for women, and less than 450 mIU/L for men / basal, fasting, morning PRL level (normal
<20mg/L) - >100-200mg/L in a nonpregnant woman indicates a need for MRI of the pituitary
-Is a common clinical problem in women and causes the syndrome of galactorrhea-amenorrhea, although hyperprolactinemia is
also seen in men, gynecomastia and especially galactorrhea are very rare
-Autonomous production of prolactin occurs with pituitary adenomas (prolactinomas) are the most common functioning
pituitary adenomas, accounting for 60% of all pituitary tumors (they are usually microadenomas when they occur in women
and macroadenomas in men), usually presenting with visual field deficits
-Signs & Symptoms :
+In women
.presents with galactorrhea
.menstrual abnormalities (amenorrhea, oligomenorrhea)
.osteoporosis in long-standing cases
.infertility
.gynecomastia
.women are detected earlier because of menstrual symptoms. Hence microadenomas are more common in women
+In men
.present with hypogonadism
.erectile dysfunction
.decreased libido
.infertility
.gynecomastia
+Usually presenting with visual field deficits
-Causes :
.pregnancy, breast-feeding or lactation, early nursing
.drugs M.C.C (with decreased inhibitory action of dopamine and overcome the normal dopamine inhibition can lead to
hyperprolactinemia) – with the use of drugs that block dopamine synthesis (phenothiazines, metoclopramide) and dopamine-
depleting agents (alpha-methyldopa, reserpine) (antidepressants, narcotics, cocaine, SSRIs and risperidone)
.micro-macroadenoma
.prolactinoma
.polycystic ovary syndrome
.nipple stimulation
.oral contraception
.pituitary adenomas (pituitary tumor)
.seizure, exercise, sleep, stress, surgery, trauma
.cirrhosis
.chronic renal failure CRF
.hypothalamic disease - hypothyroidism
+Intrauterine contraceptive device is NOT (Just Oral Contraceptive)
+Check the TSH in Pts. with elevated prolactin
*Acromegaly
-Is a syndrome that results when the anterior pituitary gland produces excess growth hormone GH (this disease is due to
hypersecretion of GH from a pituitary tumor)
+It presents between 30-50 yrs old / is an insidious, chronic debilitating disease associated with bony and soft tissue over-
growth
+In children this is called gigantism
-Signs & Symptoms :
.features of a pituitary tumor (hypopituitarism + local mass effect)
.skeletal soft tissue changes
.enlargement of the hands, feet, nose, lips and ears, and a general thickening of the skin
.soft tissue swelling of internal organs
.generalized expansion of the skull at the fontanelle
.pronounced lower jaw protrusion (prognathism) with attendant macroglossia (enlargement of the tongue) and teeth spacing
82
*Hypopituitarism
-Is the decreased (hypo) secretion of one or more of the eight hormones normally produced by the pituitary gland at the base
of the brain. If there is decreased secretion of most pituitary hormones, the term panhypopituitarism (pan meaning "all") is
used
+Sheehan's Syndrome
-also known as Simmonds syndrome, postpartum hypopituitarism or postpartum pituitary gland necrosis, is hypopituitarism
(decreased functioning of the pituitary gland), caused by ischemic necrosis due to blood loss and hypovolemic shock during and
after childbirth
-Signs & Symptoms :
.galactorrhea (absence of lactation) and/or difficulties with lactation
.amenorrhea or oligomenorrhea after delivery
.loss of secondary sexual characteristics
.infertility
+Woman with Sheehan syndrome might be relatively asymptomatic
.secondary hypothyroidism
.tiredness
.intolerance to cold
83
.hypotension
.constipation
Page
.weight gain
.hair loss
.slowed heart rate
.low blood pressure
.secondary adrenal insufficiency
.in the rather chronic case is similar to Addison's disease with symptoms including fatigue, weight loss, hypoglycemia (low blood
sugar levels)
.anemia
.hyponatremia (low sodium levels)
.syndrome of inappropriate antidiuretic hormone (ADH) hypersecretion
.decreased free-water clearance by glucocorticoid deficiency (independent of ADH)
-Causes :
.after excessive blood loss (complication of pregnancy) (postpartum hemorrhage. it is 1 st symptom and lead to failure of
lactation)
.disseminated intravascular coagulation (i.e., in amniotic fluid embolism or HELLP syndrome)
+People with diabetes are recommended to have their albumin levels checked annually, beginning immediately after diagnosis
for type 2 diabetics, and five years after diagnosis for type 1 diabetics
Page
-Treatment :
.ACE inhibitor medications (which usually reduce proteinuria levels and slow the progression of diabetic nephropathy)
.control of high blood pressure and blood sugar levels
.reduction of dietary salt intake
*Diabetes Insipidus DI
-Is a condition characterized by excessive thirst and excretion of large amounts of severely diluted urine (>3L/day)
-Types :
.central DI (M.C type in humans) (caused by a deficiency of vasopressin, also known as antidiuretic hormone ADH)
nd
.nephrogenic diabetes insipidus - genetic (2 M.C type) (caused by an insensitivity of the kidneys to ADH)
-Signs & Symptoms :
.polyuria – excessive urination (production of abnormally large volumes of dilute urine)
.polydipsia – extreme thirst (especially for cold water and sometimes ice or ice water. Are typical for DI)
.dehydration
.hypernatremia
.fever
.vomiting or diarrhea
.in children (DI can interfere with decreased appetite, weight loss, dec. growth)
-Causes :
.idiopathic
.congenital
.tumors (craniopharyngioma, metastasis, pituitary tumor)
.trauma (head injury)
.sarcoidosis
.vascular (sheehan`s syndrome, haemorrhage)
.infection (meningoencephalitis)
.drugs (lithium, demeclocycline, chronic renal disease, post-obstructive uropathy)
.occurs in histiocytosis
.can be familial disease
.can cause failure to thrive
.can cause developmental delay
-Diagnosis :
.fluid deprivation test (BEST)
.urinalysis (urine osmolarity and electrolyte levels are typically low)
-Classification :
.neurogenic (known as central DI, is due to a lack of vasopressin production in the brain)
.nephrogenic (is due to the inability of the kidney to respond normally to vasopressin)
.lithium toxicity and hypercalcemia
-Treatment :
.central DI respond to desmopressin (will be ineffective in nephrogenic DI, and you can use thiazide)
.Hyporeflexia
.Ataxia
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.Pathological reflexes
.Tremor
.Asterixis
+Respiratory
.Cheyne-Stokes respiration
+Neurological
.Dysarthria
.Lethargy
.Confusion
.Delirium
.Seizures
.Coma (from cerebral edema)
-Causes :
.infections (Meningitis, Encephalitis, brain abscess, rocky mountain spotted fever, AIDS)
.trauma, Subarachnoid hemorrhage, subdural hematoma, cavernous sinus thrombosis
.hydrocephalus
.Guillain-Barré syndrome
.multiple sclerosis
.cancers (carcinomas, lung cancer ‘small-cell lung cancer, mesothelioma’, GI cancers ‘stomach, duodenum, pancreas’,
genitourinary cancers, bladder, urethral, prostate, endometrial’)
.lymphoma
.sarcomas (Ewing's sarcoma)
.pulmonary causes (pneumonia, lung abscess)
.asthma
.cystic fibrosis
.transient causes (endurance exercise, general anesthesia)
.hereditary causes
.sarcoidosis
+Drugs Can Cause SIADH :
.Chlorpropamide
.Ciprofloxacin
.Clofibrate
.Moxifloxacin
.Phenothiazine
.Ifosfamide
.Cyclophosphamide
.Carbamazepine
.Oxcarbazepine
.Valproic Acid
.Selective serotonin reuptake inhibitors (SSRIs, a class of antidepressants)
.3,4-Methylenedioxymethamphetamine (MDMA, commonly called Ecstasy). SIADH due to taking ecstasy was cited as a factor in
the death of Leah Betts)
.Oxytocin
.Vincristine
.Morphine
.Amitriptyline
+Can Present With :
.Decreased serum osmolality
.Decreased serum sodium
.Increased urine sodium
.Increased urine osmolality
+Laboratory Findings In Diagnosis Of SIADH :
.Euvolemic hyponatremia <134 mEq/L, POsm <275 mOsm/kg OR
.Urine osmolality >100mOsm/kg of water during hypotonicity
.Urine sodium concentration >40 mEq/L
86
*Gastrinoma
-Is a tumor in the pancreas or duodenum that secretes excess of gastrin leading to ulceration in the duodenum, stomach and
the small intestine. There is hypersecretion of the HCl acid into the duodenum, which causes the ulcers. Excessive HCl acid
production also causes hyperperistalsis, and inhibits the activity of lipase, causing severe diarrhea
+It is frequently the source of the gastrin in Zollinger-Ellison syndrome / G cell (gastrin)
+It is usually found in the duodenum, although it may arise in the stomach or pancreas. Those occurring in the pancreas have a
greater potential for malignancy
+Most gastrinomas are found in the gastrinoma triangle; this is bound by the junction of cystic and common bile ducts, junction
of the second and third parts of the duodenum, and the junction of the neck and body of the pancreas
+Gastrinomas are rare endocrine tumors and commonly present with severe recurrent peptic ulcer disease
87
+More than 60% of gastrinomas are malignant and multifocal (multiple) / M.C site is pancreas, 2 nd M.C is duodenum
-Signs & Symptoms :
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.hypergastrinemia
.ulcers of the duodenum, stomach, and small intestine
.severe diarrhea
.generalized cancer symptoms
-Diagnosis :
.fasting serum gastrin
.in case of moderate hypergastrinemia, a secretin stimulation test can help in the diagnosis
.localization by somatostatin scintigraphy
-Treatment :
.proton pump inhibitors
.surgery
*Diabetic Foot
-Is a foot that exhibits any pathology that results directly from diabetes mellitus or any long-term (or "chronic") complication of
diabetes mellitus
+Local trauma and often in association with lack of sensation because of neuropathy in addition to microvascular disease, may
lead to a diabetic foot infection
+Presence of several characteristic diabetic foot pathologies such as (infection, diabetic foot ulcer and neuropathic
osteoarthropathy is called diabetic foot syndrome)
+Blood sugar control is the best way to prevent diabetic foot infection
-Treatment :
.antibiotics
.surgical debridement
.insulin
.limb elevation
**Thyroid Gland
*Hyperthyroidism (Thyrotoxicosis)
-Excess synthesis and secretion of thyroid hormone by the thyroid / Excess production of TSH “rare” or abnormal thyroid
stimulators. Amiodarone can induce thyrotoxicosis
-Types :
.diffuse toxic goiter (Graves disease) (M.C.C)
.toxic multinodular goiter (Plummer disease) (occurs in 15-20% of Pts. with thyrotoxicosis. Occurs more commonly in elderly
individuals)
.toxic adenoma (is caused by a single hyperfunctioning follicular thyroid adenoma)
+The hypermetabolic effect of thyrotoxicosis affects every organ system
+All thyroid disease occur more frequently in women than in men (F > M)
-Signs & Symptoms :
.nervousness
.anxiety
.increased perspiration (sweating)
.tremor
.hyperactivity, hyperreflexia
.palpitations
.weight loss, increased appetite
.reduction in menstrual flow or oligomenorrhea (infertility)
.tachycardia or atrial arrhythmia
.systolic hypertension
.warm, moist, smooth skin
.lid lag
.exophthalmos (stare)
.muscle weakness
.heat intolerance
.diarrhea
88
.irritability
.emotional lability
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.itchy
+Other Causes Of Thyrotoxicosis :
.struma ovarii is ectopic thyroid tissue associated with (dermoid tumors or ovarian teratomas)
.Pts. with a molar hydatidiform pregnancy or choriocarcinoma have extremely high levels of beta human chorionic
gonadotropin (beta-hCG), which can weakly activate the TSH receptor
+Graves` Disease
-M.C.C of hyperthyroidism in Pt. under age 50yrs F > M / Decreased TSH – Increased T4-T3 / Diffusely enlarged thyroid
-Graves` disease or toxic diffuse goiter = hyperthyroidism + diffuse goiter + exophthalmos + dermopathy
+This is autoimmune disorder (antibody against TSH receptor) caused by stimulatory TSH-receptor antibodies
+It is associated with other autoimmune disease (pernicious anemia, myasthenia gravis, vitiligo, type 1 DM, addison`s disease,
adrenal insufficiency)
-About Grave's Disease (Thyrotoxicosis) :
st
.eye disease (may be the 1 sign of G.d - exophthalmos)
.increased pulse
.tremor
.palmar erythema
.hair thinning
.lid lag
.lid retraction
.goitre
.pretibial myxoedema
.oedematous swelling
.above lateral malleolus
.thyroid acropachy (clubbing, painful finger and toe swelling)
.mild normocytic anaemia
.leucopenia, Ca+2 increased, LFT increased
.myopathy
.atrial fibrillation
-Treatment of thyrotoxicosis :
.Neomercazole
.Radioactive iodine
.Surgery
.Propranolol inderal
.Carbimazole
.Potassium perchlorate
.Propranolol
-Differential Diagnosis :
.acromegaly
.neurosis, anxiety
.pheochromocytoma
.cardiac disease
.ophthalmoplegia and exophthalmos
-Complications :
.unilateral (hoarseness of voice)
.bilateral (respiratory obstruction)
.heart failure (thyrotoxic cardiomyopathy)
.angina
.osteoporosis
.ophthalmopathy
.gynaecomastia
.thyroid storm
-Diagnosis :
.TSH level
89
*Hypothyroidism (Myxoedema)
-Primary hypothyroidism can occur secondary to chronic thyroiditis (Hashimoto's disease); this is the M.C.C of goitrous
hypothyroidism
-Signs & Symptoms :
.cold intolerance (increased sensitivity to cold)
.constipation
.weight gain (loss appetite and weight increased)
.fatigue, tiredness
.water retention
.bradycardia
.decreased sweating
.muscle cramps and joint pain
.dry hair – dry skin (especially on the face), itchy skin
.thin, brittle fingernails
.depression
.poor muscle tone (muscle hypotonia)
.menorrhagia (or abnormal menstrual cycle - any problems with menstrual cycles) – female infertility
.elevated serum cholesterol
.hoarse voice, slow speech
.thinning of the outer third of the eyebrows (sign of hertoghe)
.sluggish reflexes (hyporeflexia)
.deafness
.poor cognition, dementia
.myalgia
.hyponatremia
.anemia
.cerebral ataxia
.non-pitting edema
.carpal tunnel syndrome
.peripheral neuropathy
90
.lethargy
.cretinism (in the newborn)
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.pleural effusion
.periorbital puffiness
.Pericardial effusion
-Causes :
.iodine deficiency (M.C.C of hypothyroidism worldwide)
.Hashimoto's thyroiditis (M.C.C in developed countries – JORDAN)
.primary hypothyroidism (lymphocytic infiltration of the thyroid)
.secondary hypothyroidism (from hypopituitarism ) is very rare
-Diagnosis :
.in primary (increased TSH – decreased T4)
.in secondary (decreased or normal TSH – decreased T4)
+Associations :
.turner's syndrome
.down's syndrome
.cystic fibrosis
.primary biliary cirrhosis
.medullary carcinoma
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**Parathyroid Glands
*Hyperparathyroidism
-Is overactivity of the parathyroid glands resulting in excess production of parathyroid hormone (PTH). The parathyroid
hormone regulates calcium and phosphate levels and helps to maintain these levels
+Primary (M.C)
-Primary hyperparathyroidism results from a hyperfunction of the parathyroid glands themselves
-Over secretion of PTH due to :
.parathyroid adenoma
.parathyroid hyperplasia
.rarely, a parathyroid glands carcinoma
+Secondary
-Secondary hyperparathyroidism is due to physiological secretion of parathyroid hormone (PTH) by the parathyroid glands in
response to hypocalcemia (low or normal blood calcium levels). The M.C.C are Vit D deficiency and chronic kidney failure
+Vit D deficiency lead to absorption of Ca+2 from GI
+2 +2
+PTH (parathyroid hormones) lead to increased Ca / Calcitonin (thyrocalcitonin – parafollicular cells) lead to decreased Ca
-Signs & Symptoms :
.weakness, fatigue
.depression
.bone pain
.muscle soreness (myalgias)
.decreased appetite
.vomiting, nausea
.constipation
.polyuria
.polydipsia
.cognitive impairment
.kidney stones, renal osteodystrophy
.osteoporosis, pathologic fractures, osteomalacia, rickets
.racquet nails (trachyonychia)
.Parathyroid adenomas (very rarely detectable on clinical examination)
+In Hyperparathyroidism
.In primary hyperparathyroidism, parathyroid hormone (PTH) levels will be either elevated or "inappropriately normal" in the
presence of elevated calcium
.In cases of primary hyperparathyroidism or tertiary hyperparathyroidism heightened PTH leads to increased serum calcium
(hypercalcemia)
.In primary hyperparathyroidism, serum phosphate levels are abnormally low as a result of decreased renal tubular phosphate
reabsorption
.Alkaline phosphatase levels are usually elevated in hyperparathyroidism
*Hypoparathyroidism
-Is decreased function of the parathyroid glands with underproduction of parathyroid hormone. This can lead to low levels of
calcium in the blood. Often causing cramping and twitching of muscles or tetany (involuntary muscle contraction)
-Signs & Symptoms :
.low blood calcium level
.normal muscle contraction
.nerve conduction
.paresthesia
.fatigue
.headaches
.bone pain
.insomnia
.crampy abdominal pain
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*Hypercalcemia
-Calcium is absorbed from the proximal portion of the small intestine (duodenum)
-Signs & Symptoms :
.neurologic – result in decreased mental activity such as (lethargy and confusion)
.gastrointestinal – result in decreased bowel activity such as (constipation, anorexia, nausea, vomiting, severe pancreatitis ,UD)
.renal – result in (polyuria and polydipsia)
.cardiovascular – (hypertension and will show in ECG ‘short QT’)
-Causes :
.hyperparathyroidism (M.C.C)
.sarcoidosis
.TB
.malignancy
.Vit D intoxication
.thiazide
.lithium
.paget's disease
*Hypocalcemia
-Signs & Symptoms :
.seizures
.tetany
.numbness and tingling of the extremities
.arrhythmias (because of a prolonged QT)
-Causes :
.hypoparathyroidism (M.C.C)
.massive blood transfusion
.renal failure
.hypomagnesemia
.hyperphosphatemia
.alkalosis
.drugs such as (loop diuretics, phenytoin, alendronate and doscarnet)
-Is a group of metabolic diseases in which there are high blood sugar levels over a prolonged period, diabetes is due to either
the pancreas not producing enough insulin or the cells of the body not responding properly to the insulin produced
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-Characterized by chronic hyperglycemia due to relative or absolute deficiency of insulin secretion, insulin action, or both
+Insulin Deficiency Lead To
.disturbance of carbohydrate, fat and protein metabolism
.significant disturbance of water and electrolyte homeostasis
+There Is Also
.microvascular complication (diabetic nephropathy, retinopathy)
.macrovascular complication (increased prevalence of coronary artery disease, peripheral vascular disease and strokes)
.autonomic neuropathy
-Classification :
A) Primary
.type 1 (or insulin dependent diabetes mellitus IDDM)
.type 2 (or non insulin dependent diabetes mellitus NIDDM)
B) Secondary
.genetic defects (defect in beta cell function / abnormal insulin action)
.pancreatic disease (pancreatitis, pancrectomy, hemochromatosis, cystic fibrosis, neopalstic disease)
.endocrinal disease (excess endogenous production of hormone antagonist to insulin – Counter-regulatory hormones)
(GH – acromegaly / Glucocorticoids – Cushing`s syndrome / Thyroid hormone – Thyrotoxicosis / Catecholamines –
Pheochromocytoma / Glucagon – Glucagonoma / Human placental lactogen HPL – Pregnancy)
*NB. : Counter-regulatory hormones increase in severe burn and trauma
.viral infections (congenital rubella, mumps, coxasackie virus B)
.drugs (corticosteroids, thiazide diuretics, phenytoin)
.associated with genetic syndromes (Wolfram`s syndrome ‘DIDMOAD’ – Diabetes insipidus, DM, Optic atrophy, Deafness /
Down`s syndrome / Klinefelter`s syndrome / Turner`s syndrome / Friedreich`s ataxia / Muscular dystrophy / Lipoatrophy)
C) Gestational Diabetes Mellitus
.any degree of glucose intolerance with the onset or first recognition during pregnancy
.diagnosis (screening at 24-28wks of gestation / FBG>126 or casual glucose >200 / plasma glucose 1hr after 5mg oral glucose
if glucose >140 mg/dl perform oral glucose tolerance test OGTT fasting >95, 1hr >180, 2hr >155, 3hr >140)
*NB. : tow or more must be met for diagnosis
-Types :
*Type 1 DM (IDDM-insulin dependent)
-”Type 1 diabetes” has replaced several former terms, including (childhood-onset diabetes, juvenile diabetes, and insulin-
dependent diabetes mellitus). May occur at any age
-Causes :
.genetic susceptibility (account for 1/3 susceptibility to type 1 DM, 90% of type 1 DM Pts. carry HLA-DR 3 or DR4 compared with
40% of the general population)
.environmental factor (viruses – mumps, coxsackie`s virus, retroviruses, rubella, CMV, EBV) (Diet – bovine serum albumin BSA
from cow`s milk, nitrosamines “found in smoked and cured meat” and coffee are potentially diabetogenic factor, dietary
proteins) (stress) (immunological factors – IDDM is slow T cell-mediated autoimmune disease in which insulin-secreting cells)
*NB. : Children who are given cow`s milk early in infancy are more likely to develop IDDM than those who are beast fed
-Characterized by :
.loss of the insulin-producing beta cells of the islets of langerhans in the pancreas, leading to insulin deficiency
.the majority of type 1 diabetes is of the immune-mediated nature
.there is no known preventive measure against type 1 diabetes
.Pt. always need insulin and prone to ketoacidosis and wight loss
.it is associated with other autoimmune diseases (HLA-B8 / HLA-B15 / HLA-DR3 / HLA-DR4)
+Cause of IDDM (loss of the insulin-producing beta cells of the islets of langerhans in the pancreas)
+(Younger Pt. / HLA-D3 & D4 linked / Autoimmune beta cell destruction / Polydipsia, polyuria, weight loss, ketoacidosis)
metabolic functions so predisposing to type 2 DM) (Age – is a disease of middle aged and elderly, affecting 10% of the
population over age of 65) (pregnancy – insulin sensitivity is reduced through action of placental hormones and his affect
glucose tolerance)
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-Characterized by :
.insulin resistance
.reduced insulin sensitivity
.usually maturity onset (M > F), most Pts. are over 40yrs
.strong family history of diabetes
.it is associated with obesity and lack of exercise and calorie excess
+Causes of NIDDM (decreased insulin secretion, increased insulin resistance)
+(Older Pt. / No HLA association / Insulin resistance / Often asymptomatic, present with micro- or macrovascular complications)
Type 1 DM Type 2 DM
Age of onset <40yrs >40yrs
Duration of symptoms Weeks Weeks to months
Body weight Normal or wasted Obese
Plasma insulin Low to absent Normal to high
Acute complications DKA Hyper-osmolar coma
Insulin therapy Responsive Responsive to resistant
Oral therapy Non-responsive Responsive
Auto-antibodies (islet cell Ab) Yes (common) No (rare)
Associated with other autoimmune Yes No
disease
Ketouria Yes No
Rapid death without trt with insulin No Yes
Family history of DM No Yes
Diabetic complications at diagnosis No Yes
Onset Sudden Gradual
Ketoacidosis Common Rare
Prevalence 10% 90%
+Microvascular disease
.diabetic retinopathy (deterioration of vision)
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*Hypoglycemia
-This is the commonest endocrine emergency / brain damage and death can occur in severe prolonged cases
-Signs & Symptoms :
96
.sweating
.drowsiness
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.seizures
.coma
.decreased level of consciousness
.tachycardia
.tremor
.palpitation
.visual changes
.brain death
-Causes :
.improper insulin use
.insulinoma
.hypoadrenalism
.paracetamol overdose
.alcohol
.postprandial
.hepatic failure
.glibenclamide therapy
.addison's disease
-Treatment :
.glucose water
*Fasting Hypoglycemia
-Causes :
.exogenous drugs
.pituitary insufficiency
.liver failure (enzyme defects)
.Addison's disease
.islet cel tumours (insulinoma, hodgkin's disease)
.non-pancreatic neoplasms
.hyperinsulinism (can occur secondary to insulinoma)
*Post-Prandial Hypoglycaemia
-May occur after gastric surgery and in type 2 diabetes
*MEN Type 1
-The gene defect in MEN type 1 (Chromosome 11)
-The M.C tumors (PPPs) :
.parathyroid hyperplasia (M.C)
.pancreatic islet cell tumors (gastrinoma ‘ZES’, insulinoma) (M.C gastrinoma)
.pituitary tumors (M.C prolactinoma)
.adrenal and thyroid adenomas
*MEN Type 2A
-The gene defect in MEN Type 2 (RET)
-The M.C tumors :
.medullary thyroid carcinoma
.pheochromocytoma
.hyperparathyroidism (hypercalcemia)
*MEN Type 2B
-The M.C abnormalities :
.mucosal neuromas (in the nasopharynx, oropharynx, larynx and conjunctiva)
97
.pheochromocytoma
+The M.C GI complaint of Pts. with MEN-2B (Constipation)
-The major difference between MEN-2A and MENT-2B :
.MEN-2A (parathyroid hyperplasia)
.MEN-2B (NO parathyroid hyperplasia)
**Thyroid Cancer
-Most often the first symptom of thyroid cancer is a nodule in the thyroid region of the neck (Typically under 5% of these
nodules are found to be malignant) (Thyroid cancer usually found in a euthyroid Pt.)
-To achieve a definitive diagnosis before deciding on treatment (Fine needle aspiration FNA)
-Types Of Thyroid Carcinoma :
.papillary carcinoma (M.C)
.follicular carcinoma
.medullary carcinoma
.hurthle cell carcinoma
.anaplastic/undifferentiated carcinoma
+Oncogenes are associated with thyroid cancers (Ras gene family and RET proto-oncogene)
*Thyroid Nodules
-The Differential Diagnosis Of A Thyroid Nodule :
.multinodular goiter
.adenoma
.hyperfunctioning adenoma
.cyst
.thyroiditis
.carcinoma/lymphoma
.parathyroid carcinoma
+The diagnostic test of choice for thyroid nodule (FNA)
+The M.C.C of thyroid enlargement (Multinodular goiter)
*Papillary Carcinoma
-M.C type / F > M, usually affect young females / Excellent prognosis
-Risk factors is radiation
-Metastasis (M.C site is lymph node)
*Follicular Adenocarcinoma
-The route of spread (Hematogenous, more aggressive than papillary adenocarcinoma) (M > F)
-Metastasis (M.C site is bone)
*Medullary Carcinoma
-Associated (MEN type 2; autosomal-dominant genetic transmission)
*Thyroiditis
-The features of acute thyroiditis :
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.painful
.swollen thyroid
.fever
.overlying skin erythema
.dysphagia
+The cause of acute thyroiditis (Bacteria ‘Streptococcus of Staphylococcus’)
-The features of subacute thyroiditis (De Quervain`s thyroiditis) :
.glandular swelling
.tenderness
.often follows URI
.elevated ESR
+The cause of subacute thyroiditis (Viral infection)
-Types of chronic thyroiditis :
.hashimoto`s thyroiditis (M.C.C of hypothyroidism)
.riedel`s thyroiditis
-The features of Hashimoto`s (chronic) thyroiditis :
.firm and rubbery gland
.F > M
.lymphocyte invasion
+The etiology of Hashimoto`s disease (Autoimmune)
-Tests you should be performed to diagnose Hashimoto`s disease :
.antithyroglobulin
.microsomal antibodies
.psychiatric symptoms
.ecchymosis
.immune suppression
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.C-21 (hydroxylase deficiency) – is associated with reduction in aldosterone secretion in one third of Pts (CAH is associated with
virilization) (Pts. may be male at birth with macrogenitosomia)
.C-11 (hydroxylase deficiency) – this can lead to hypertension and hyperkalemia
.C-17 (hydroxylase deficiency) – is characterized by hypogonadism, hypokalemia and hypertension
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**Adrenal Insufficiency
*Primary Adrenocortical Insufficiency (Addison's Disease)
-Is a rare, chronic endocrine system disorder in which the adrenal glands do not produce sufficient steroid hormones
(glucocorticoids ”cortisol” and mineralocorticoids “aldosterone”)
+Resulting from adrenocortical hypofunction (adrenal insufficiency post-bilateral adrenalectomy)
-Addison's disease is associated with the development of other autoimmune diseases, such as type 1 diabetes, thyroid disease
(Hashimoto's thyroiditis) and vitiligo
-Signs & Symptoms :
.sudden penetrating pain in the legs, lower back or abdomen
.severe vomiting and diarrhea, resulting in dehydration
.low blood pressure
.syncope
.confusion, psychosis, slurred speech
.severe lethargy
.hypoglycemia
.hyponatremia
.hyperkalemia
.hypercalcemia
.convulsions
.fever
.weight loss
.nausea, vomiting
.axillary hair loss
.hyperpigmentation of the skin
.ACTH is high
.causes small heart
.may be secondary to tuberculosis
.fatigue, weakness, anorexia, weight loss, dizziness
-Treatment :
.IV fluids
.IV steroids
*Pheochromocytoma PCC
-Is a rare tumor of adrenal gland tissue (neuroendocrine tumor of the medulla of the adrenal glands)
+It results in the release of too much (secretes excessive amounts of) catecholamines, usually epinephrine-adrenaline and
norepinephrine-noradrenaline, hormones that control heart rate, metabolism, and blood pressure
+It usually develops in the center (medulla) of one or both adrenal glands and associated with paroxysmal hypertension
-Signs & Symptoms :
.abdominal-chest pain
.irritability, anxiety
.nervousness
.pallor
.palpitations
.rapid heart rate (tachycardia)
.severe headache
.sweating (diaphoresis)
.weight loss
.hand tremor
.high blood pressure (HTN)
.sleeping difficulty
.seizures
.visual disturbances
.nausea
101
.constipation
-Diagnosis :
.urinary metanephrine
Page
.hypokalaemia
.hypomagnesaemia
.hypophosphatemia
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.hypoglycaemia
.hyponatremia
.thrombo-embolism
.hyperosmolar non-ketotic coma
.Increased anion gap
.Pseudohyponatremia
2
.Paco decreased
.PH decreased
.leukocytosis
-Treatment :
.give K
.monitor intake – output
.correct acidosis when pH is less than 7.1
.monitoring ketones in the blood is more important than in urine
.heparin may be used prophylactically
DKA HONK
Age Any >60yrs
Mortality 5% 40%
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**Insulinoma
-Is a tumor of the pancreas that produces excessive amounts of insulin / The tumor are usually small (<2cm) and solitary (single)
and may not appear on CT
-Pancreatic B-cell tumor and associated with MEN-1, can cause hypoglycemia-benign tumors
-Signs & Symptoms :
.subacute or chronic hypoglycemia (low blood sugar)
.blurred vision
.headache
.feeling of detachment
.slurred speech
.weakness
.symptoms occur in the early morning or late afternoon or after fasting or exercise
-Diagnosis :
.by measurements of blood sugar and insulin level in the blood (8 mg/mL or more in the presence of blood glucose values <40
mg/dL)
.CT scan,U/S and arteriography may also be useful in detecting the tumors
-Treatment :
.enucleation (surgical removal of a mass without cutting into or dissecting it) (BEST)
**Glucagonoma
-Is a rare tumor of the alpha cells of the pancreas, that results in the overproduction of the hormone glucagon
-Signs & Symptoms :
.DM (present in 80-90% of cases of glucagonoma - not responding to insulin)
.high blood glucose levels
.activation of anabolic and catabolic processes (gluconeogenesis and lipolysis)
.decreased blood levels of amino acids (hypoaminoacidemia)
.anemia
.diarrhea
.weight loss of 5–15 kg
.necrolytic migratory erythema NME (hyperglucagonemia)
+NME is a red, blistering rash that spreads across the skin. It particularly affects the skin around the mouth and distal
extremities; but may also be found on the lower abdomen, buttocks, perineum, and groin. It is strongly associated with
glucagonoma, a glucagon-producing tumor of the pancreas, but is also seen in a number of other conditions including liver
disease and intestinal malabsorption
-Diagnosis :
.blood serum glucagon (1000 pg/mL or greater is indicative of glucagonoma (the normal range is 50–200 pg/mL)
.plasma glucagon levels (ranging from 500 to 1000 pg/mL)
+Increased levels have been reported in cases of (decreased kidney function, acute pancreatitis, hypercorticism, liver diseases,
severe stress, extended fasting, and familial hyperglucagonemia)
.blood tests (may also reveal abnormally low concentrations of amino acids, zinc, and essential fatty acids)
.skin biopsies (may also be taken to confirm the presence of NME)
.CBC (low level of hemoglobin)
.MRI, CT
-Treatment :
.octreotide (somatostatin analog – inhibits GI secretion, which inhibits the release of glucagon)
+Only curative therapy for glucagonoma is surgical resection
**Adrenal Cortex
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**Gynecomastia
-Is a common endocrine disorder in which there is a benign enlargement of breast tissue in males
+Decreased testosterone production and relatively high estrogen levels, leading to gynecomastia
-Causes :
.Physiologic (M.C)
.cirrhosis of the liver
.bronchogenic carcinoma
.testicular atrophy
.digitalis therapy
.old age
.hyperthyroidism (hyperparathyroidism is not) - hyperprolactinemia
.spironolactone, calcium channel blockers (used to treat HTN) (nifedipine, ketoconazole, methyldopa, cimetidine, digitoxin)
.drugs of abuse (alcohol, marijuana, heroin)
.puberty
.bronchogenic carcinoma
.klinefelter's syndrome
.testicular cancers
.CRF
.digoxin therapy
**Raynaud's Phenomenon
-Vasospastic disorder causing discoloration of the fingers, toes, and occasionally other areas
+Primary Raynaud's (Disease) – it often develops in young women in their teens and early adulthood + cold
+Secondary Raynaud's (Syndrome) :
.scleroderma (M.C.C)
.SLE
.rheumatoid arthritis
.Sjogren's syndrome
.dermatomyositis
.polymyositis
.mixed connective tissue disease
.cold agglutinin disease
.Ehlers-Danlos Syndrome
.hypothyroidism
.arthritis
.diabetes
.pre diabetes (impaired glucose tolerance)
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.trauma
.lipomas (is a benign tumor composed of adipose tissue - body fat)
.ganglion (is a nerve cell cluster or a group of nerve cell bodies located in the autonomic nervous system)
.vascular malformation
.repetitive activities of the hand and wrist
.acromegaly (causes excessive GH)
.cardiomyopathy
.polyneuropathy
-Treatment :
.surgery
**Avitaminosis
+Vit A deficiency causes (xerophthalmia or night blindness)
+Vit B1 (thiamine deficiency) causes (beriberi)
+Vit B3 (niacin deficiency) causes (pellagra) (diarrhea, dermatitis, dementia and death)
+Vit B12 deficiency leads to (megaloblastic anemia and subacute combined degeneration of spinal cord)
+Vit C deficiency leads to (scurvy) (easy bruising and petechiae, gum disease, loosening of teeth, poor wound healing)
+Vit D deficiency causes (rickets and osteomalacia)
+Vit K deficiency causes (impaired coagulation – bleeding)
106Page
RHEUMATOLOGY
**Rheumatoid Arthritis RA
-Is a chronic, systemic inflammatory disorder that may affect many tissues and organs (multisystemic disease) / F > M (middle
age 40-50yrs) - but people of any age can be affected
+The hallmark of RA is inflammatory synovitis
+RA is considered a systemic autoimmune disease
+RA can also produce diffuse inflammation in the lungs, membrane around the heart (pericardium), the membranes of the
lungs (pleura) and white of the eye (sclera) and also nodular lesion, most common in subcutaneous tissue (DIP)
+The predominant infltrating call is the T lymphocyte (disease like HIV, in which T cells are decreased, will characteristically
improve preexisting RA; this is also the reason why RA is very rare in Pts. with HIV)
-Diagnostic Criteria (neef 4 of the folloing diagnostic criteria) :
.morning stiffness (>1h) (improve with movement of joint)
.>6wks symptoms
.symmetrical (bilateral)
.mainly affect small joints of hand and wrist
.>2 joints affected
.deforming arthritis
.swelling of wrists, MCPs, PIPs (for 6 wks)
.swelling of three joints (for 6 wks)
.joint erosion on x-ray
.RF positive
.rheumatoid nodules
+Summary of Criteria :
.RA is a chronic inflammatory symmetric arthropathy
.some joints are never involved in RA (DIPs – joints of the lower back) (DON'T affect distal interphalangeal joint)
.because RA is a systemic disease, tow-thirds of the Pts. present with constitutional symptoms (fatigue, anorexia, weight loss,
weakness-before the onset of the arthritis)
+Deformity Of Hand In RA :
.swan neck deformity
.Z-thumb
.wrist subluxation
.ulnar deviation
+Falty syndrome (RA, splenomegaly, neutropenia)
+Caplan syndrome (RA, pneumoconiosis)
-Signs & Symptoms :
+Joints (known as synovitis) - is inflammation of the synovial membrane that lines joints
.joint become swollen, tender and warm, and stiffness limites their movement
.the affected joints being swollen, warm, painful and stiff, particularly early in the morning on waking or following prolonged
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.anemia
.ESR or CRP is high
.X-ray
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+Cardiac
.pericarditis
.myocarditis
.endocarditis
.Noninfective (libman-sacks endocarditis)
+Pulmonary
.pleuritis
.pleural effusion
+Renal
.hematuria
.proteinuria
.acute or end stage renal failure
+Neurological
.headache
.depression
.seizures
.cognitive dysfunction
.mood disorder
.cerebrovascular disease
.polyneuropathy
.anxiety disorder
.psychosis
+Reproductive
.increased rate of fetal death in utero and spontaneous abortion
+Other
.Raynaud phenomenon
.fever
.malaise
.joint pains (myopathy)
.myalgias
.fatigue
.abdominal pain
+Signs Of Active SLE :
.anti ds-DNA antibody
.anti-smith antibody
.high EST / low CRP
.decreased C3, C4
-Diagnosis :
.a positive ANA supports the diagnosis but is not specific for SLE
.the dsDNA and anti-smith are specific antibodies for lupus (these occur only with lupus so if found, think lupus only)
.complement levels (C3, C4 or the more sensitive CH50 are decreased in Pts. with active lupus)
.elevated levels of ds-DNA antibodies when positive are seen with active lupus / the ds-DNA antibodies when positive are very
specific for diagnosis of lupus
.anti extractable nuclear antigen (anti-ENA) (serologic form testing for SLE)
+Pregnancy and SLE :
.fertility rates are normal in Pts. with SLE, but spontaneous abortions and are more common
.one reason for the spontaneous abortions in these Pts. may be anti-phospholipid antibodies, which cause placental infarcts
.this is treated with low-molecular weight heparin (LMWH) and aspirin during pregnancy
.all pregnant Pts. with lupus need to be screened for SSA/anti-Ro antibodies. These cross the placenta and are passively
transferred to the fetus, causing neonatal lupus and rarely permanent heart block
-Treatment :
.corticosteroids (cortisone) / immunosuppressive drugs / antimalarial drugs (cyclophosphamide, mycophenolate,
hydroxychloroquine)
.renal transplantation (for end-stage renal disease)
.neonatal lupus (most serious complication for neonatal lupus is heart block)
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**Scleroderma SSc
-Is a chronic systemic autoimmune disease (primarily of the skin-skin thickening) (Mainly affect skin)
+Disease characterized clinically by thickening of the skin caused by accumulation of connective tissue and by involvement of
visceral organs (GI, lungs, kidneys / example ‘scleroderma renal crisis’ - has been used to characterize the renal involvement in
scleroderma)
+F > M (to develop scleroderma)
-Diffuse :
+GI gesture include (dysphagia, GERD, malabsorption)
+Pulmonary features include (pulmonary fibrosis with restrictive lung disease, cor pulmonale) – pulmonary involvement is now
the leading cause of death in SSc
+Renal features include (the scleroderma renal crisis in wich malignant hypertension develops and causes acute renal failure) –
this way the M.C.C of death
+Heart (HTN, heart failure)
-Antibody :
+Diffuse (anti-topoisomerase antibody)
+Limited (anti-centromere antibody)
-Types :
1.limited Systemic Sclerosis (CREST syndrome – affect hand, arm, face)
.scleroderma involves cutaneous manifestation that mainly affect the (hand, arm, face) and called CREST syndrome
.Pt. with limited scleroderma (the ANA test is positive)
.Scl-70 test (anti topoisomerase antibody) is negative in limited scleroderma and positive in diffuse ascleroderma
+CREST syndrome or Limited scleroderma
.Calcinosis (calcium deposits occur in soft tissue usually in the fingers)
.Raynaud (raynaud phenomenon)
.Esophageal dysfunction
.Sclerodactery
.Telangiectasias
+Raynaud's phenomenon (Raynaud Disease) is seen in : (vasospastic disorder causing discoloration of the fingers, toes)
.SLE
.SSc
.RA
.CREST
.Thoracic outlet syndrome
.Dermatomyositis
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.Polymyositis
.Mixed connective tissue disease
.Ehlers-Danios syndrome
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**Sjogren's Syndrome
-Is a chronic autoimmune disease characterized by lymphocytic infiltration of the exocrine glands, resulting in xerostomia and
dry eyes
-Sjogren's Syndrome may be seen alone (primary) or in association with other autoimmune disease (secondary) such as RA,
primary biliary cirrhosis or SLE
-Sjogren's Syndrome progresses, it becomes a systemic disease involving major organs (lungs, kidneys, ect.) and may eventually
evolve into a lymphoproliferative disease (malignant lymphoma)
-Signs & Symptoms :
.itchy eyes
.sandy feeling under their eyes
.difficulty swallowing food
.also look for increase in dental caries and parotid enlargement
-Diagnostic tests :
.schirmer test
.ANAs will be positive and specifically anti-Ro (SSA) and anti-La (SSB)
+REMEMBER :
.all of the disease we just reviewed have an arthritis that is symmetrical and polyarticular (there are a few other disease that
may cause symmetrical polyarthropathy – know parvovirus B19 and hepatitis B) !
.RA is a disease that involves mostly the joints; the others, SLE, SSs and Sjogren's syndrome, usually have arthritis plus multiple
organ involvement
.DMARDS (methotrexate)
+Types Of Seronegative Arthropathies :
.Ankylosing Spondylitis (seronegative ‘ANA negative – RF negative’)
.Reactive Arthritis (involve lower back and sacroiliac joints) (Richter Syndrome -transformation of chronic lymphocytic leukemia
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- CLL)
.Psoriatic Arthritis (HLA-B27)
.Enteropathic Arthropathy (extra-articular manifestations – CD, UC)
.arthritis symptoms in the (distal interphalangeal articulation of hand-this is not typical of RA)
.ridging and pitting of fingernails or toenails (onycholysis), and this associated with psoriasis and psoriatic arthritis
.radiologic images indicating joint change
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*Enteropathic Arthropathy
-Occurs with ulcerative colitis and crohn disease; sometimes the arthritis occurs with flares of the inflammatory bowel disease
-The Pts. sometimes develop characteristic skin lesions: pyoderma gangrenosum and erythema nodosum
**Osteoarthritis OA
-Is the M.C joint disease in humans. The target tissue in OA is articular cartilage. OA, unlike RA, is not an inflammatory disease
+M.C joint to be affected is the knee, the 2nd M.C joint affected is the base of the thumb / in general, the major joints involved
in OA are the weight-bearing joints (hip and knee) and the small joints of the fingers (PIPs & DIPs)
-Risk Factors :
.age
.female sex
.genetic factors
.major joint trauma
.repetitive stress
.obesity
.gout
.endocrine disease (DM, acromegaly)
.deposition disease (hemochromatosis)
.exercise
-Lab tests :
.ESR and C-reactive protein (are always normal in OA) (if ESR is elevated, some other process is complicating OA, septic joints,
or it`s not OA)
.X-ray findings (osteophytes and unequal joint space)
+Bouchard`s nodes (when changes occur in the PIPs)
+Heberden's nodes (when changes occur in the DIPs)
-Diagnosis :
.clinical
.X-ray
-Treatment :
.NSAIDs
.COX-2 inhibitors (used in Pts. who are at high risk for GI complications)
.orthopedic surgery and joint arthroplasty
**Crystal-Induced Arthropathies
*Gout (podagra)
-Is a medical condition usually characterized by recurrent attacks of acute inflammatory arthritis (red, tender, hot, swollen
joints)
-The metatarsophalangeal joint MTP at r\the base of the big toe is the most commonly affected, other joints such as the heels,
knees, wrists and fingers / It may also present as tophi, kidney stones or urate nephropathy
+Acute attacks of gout rarely affect the shoulder
-Signs & Symptoms :
.recurrent attack of acute inflammatory arthritis
.pain usually begins over 2-4 hours and during the night
.elevated levels of uric acid may also lead to crystals precipitating in the kidneys,resulting in stone formation (uric acid stones)
.include a strong association with the consumption of (alcohol, fructose-sweetened drinks, meat, seafood, physical trauma,
surgery, coffe, vit C, dairy products)
.metabolic syndrome (abdominal obesity, hypertension, insulin resistance, abnormal lipid levels)
.diuretics have been associated with attacks of gout
.other medicines (niacin, aspirin ‘acetylsalicylic acid’)
.the immunosuppressive drugs (cyclosporine, tacrolimus)
-Causes :
.elevated levels of uric acid in the blood (hyperuricemia)
-Common Gout Triggers :
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*Pseudogout (CPPD)
-M.C in knee; other joints commonly affected are the (wrist, shoulder and ankle)
+Is more common in elderly population and in people who have pre existing joint damage / Is caused by Ca urate
-Metabolic Abnormalities That Are Associated With CPPD :
.hyperparathyroidism
.hemochromatosis
.hypophosphatemia
.hypomagnesemia
-Diagnosis :
.rectangular crystal
.rhomboid crystal
.positive birefringent crystals in synovial fluid evaluation
.radiography
-Treatment :
.is the same as gout
**Vasculitis Syndromes
-Vasculitis is an inflammatory process involving the blood vessels that results in decrease of the lumen diameter and eventual
ischemia of the tissues supplied
*Wegener Granulomatosis
-Is a small vessel vasculitis that can involve any organ system but mainly affects the respiratory tract (sinuses, nose, trachea and
lungs) and kidneys
+The M.C sign of wegener granulomatosis is involvement of the upper respiratory tract
-Signs & Symptoms :
.rhinitis (common sign of the disease is chronic rhinitis that does not respond to usual treatment)
.sinusitis
.nasal ulcers
.cough
.hemoptysis
.dyspnea
-Diagnosis tests :
.antineutrophil cytoplasmic antibodies (C-ANCA)
.positive ANCA test (is useful to support a suspected diagnosis of wegener g., it is never diagnostic). Also, the C-ANCA test may
be negative in some people with active wegener
.the only way to confirm the diagnosis is by performing a biopsy of an involved organ (usually the nasal septum)
-Treatment :
.is consists of high doses of corticosteroids and immunosuppressive drugs (cyclophosphamide)
*Churg-Strauss Syndrome
-This syndrome shares many of the clinical and pathologic features of PAN and can involve any organ
+The cardinal manifestations of churg-strauss syndrome are asthma, eosinophilia and lung involvement and the typical Pt. with
churg-strauss is a middle aged individual with new-onset asthma
-Signs & Symptoms :
.mononeuropathy
.transient pulmonary infiltrates on chest x-rays
.paranasal sinus abnormalities
.nasal polyps
.allergic rhinitis
.tongue numbness
.sudden loss of vision
.proximal stiffness (neck, arms, hips) due to polymyalgia rheumatica
-Diagnosis :
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**Inflammatory Myopathies
-The inflammatory myopathies are inflammatory muscle disease that present with progressive muscle weakness
+They include polymyositis, dermatomyositis (treated by steroids) and body myositis (treated by immunosuppressive)
-The diagnosis is confirmed by muscle biopsy
**Nail Clubbing
-Clubbing associated with :
+Lung Disease
.lung cancer (not seen in small cell lung cancer)
.interstitial lung disease (sarcoidosis, fibrosis)
.complicated TB
.lung abscess, empyema, bronchiectasis, cystic fibrosis
.mesothelioma of the pleura
.arteriovenous fistula or malformation
+Heart Disease
.any disease featuring chronic hypoxia
.congenital cyanotic heart disease (M.C cardiac cause) (tetralogy of fallot, transposition of great vessels)
.subacute bacterial endocarditis
.atrial myxoma (benign tumor)
+GI and hepatobiliary
.malabsorption
.CD and UC
.cirrhosis (especially in primary biliary cirrhosis)
.hepatopulmonary syndrome (a complication of cirrhosis)
+Others
.hyperthyroidism (thyroid acropachy)
.familial and racial clubbing and “pseudoclubbing”
+COPD + Asthma (Don't cause clubbing)
+Causes Of Clubbing Of Fingers :
.Subacute bacterial endocarditis
.Pulmonary abscess
.Hepatic cirrhosis
.CD / UC
.Bronchiectasis
.Infective endocarditis
.Fibrosing alveolitis
.Bronchogenic carcinoma
.Tetralogy of Fallot
.Lung fibrosis
.Mesothelioma
.Aortic aneurysm
+Clubbing is not a feature of bronchial carcinoma
**Behçet's Disease
-It causes orogenital ulceration
-Colchicine and steroids is used in the management
-Arthritis is a feature, Superior vena cava obstruction may occur, Iritis, Thrombophlebitis, Neurological complications may
occur,Genital ulceration, Erythema nodosum / (HLA-B5, B1) An association with the GIMAP (GIMAP1, GIMAP2 and GIMAP4)
+Causes (auto-inflammation of the blood vessels)
+Vitiligo is associated with :
.Addison's disease
.Pernicious anemia
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.Diabetes mellitus
.Thyrotoxicosis
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**Erythema Nodosum EN
-Is an inflammatory condition characterised by inflammation of the fat cells under the skin
+Painful rash anterior to leg (Don't ulcerate)
-Causes :
.in about 30-50% of cases, the cause of EN is unknown – idiopathic (M.C.C)
.infections (HCV, TB, Streptococcal, Mycoplasma Pneumoniae, Yersinia, EBV)
.sarcoidosis, autoimmune disorders (inflammatory bowel disease or Behcet's disease)
.pregnancy
.medications (sulfonamides, oral contraceptives, bromides, indomethacin)
.lepromatous leprosy
.RA
.arthralgia
.residual bruised appearance
.tenderness of lesions
PULMONOLOGY
**Pleural Effusion
-Is excess fluid that accumulates between the tow pleural layers, the fluid-filled space that surrounds the lungs (accumulation of
fluid in the pleural cavity)
-Lymph is aspirated from the pleural cavity in chylothorax
-Signs Of Pleural Effusion :
.stony dullness on percussion
.diminished or absent breath sound
.deviation of trachea to opposite side
.bronchial breathing above effusion
-Diagnosis :
.confirmed by chest X-ray (costophrenic angle - 1st sign on CxR)
-Types :
+Transudative (low protein <25g/L) (increased hydrostatic pressure, decreased collcid osmotic pressure)
-Causes :
.heart failure
.constrictive pericarditis
.fluid overload
.meigs syndrome (ovarian fibroma + Rt. pleural effusion)
.nephrotic syndrome
.liver disease (cirrhosis)
.pulmonary embolism
.atelectasis
-Diagnosis :
.protein <25g/L (serum ratio <0.5)
.LDH <200 IU/ml (serum ratio <0.6)
.clear
-Treatment :
.chest tube
.tetracycline, bleomycin (pleurodesis)
.surgery
+Exudative (high protein 95g/L) (inflammation)
-Causes :
.bacterial pneumonia - empyema (parapneumonic effusions) (M.C.C of exudative pleural effusion)
.cancer (lung cancer, breast cancer and lymphoma - M.C.C of malignant pleural effusion)
.TB
.pulmonary embolism
.collagen vascular disease (RA, SLE)
118
.drug induced
.pancreatitis
-Diagnosis :
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**Obstructive Diseases (Obstructive Lung Disease – COPD, Asthma, Bronchiectasis, Cystic Fibrosis)
*Asthma
-Is the common chronic inflammatory disease of the airways, characterized by variable and recurring symptoms, reversible
airflow obstruction and bronchospasm (hyperreactivity of the respiratory tree to various stimuli, resulting in reversible airway
obstruction)
+Differentiates the asthma from COPD (Variability)
+Atopic Asthma (children – increased IgE) / Non-atopic Asthma (>40yrs – IgE normal)
+Pathophysiology :
.airway airway hyperresponsiveness (variability)
.bronchospasm
.inflammation (increased eosinophils)
.increased mucus production
-Signs & Symptoms :
.cough (M.C symptom)
.urticaria, allergic rhinitis and eczema
.wheezing
.shortness of breath (dyspnea)
.chest tightness and coughing
.worse at night or in the early morning or in response to exercise or cold air
.low PO2
.pulsus paradoxus
.cyanosis (severe asthma)
.restlessness
.silent chest (severe asthma)
.tachycardia (more than 130 per min)
.hypercapnia
+bradycardia and pulsus alternans are NOT
-Causes :
+Intrinsic (non-allergic) / Extrinsic (allergic)
.genetic factors (atopic, allergic – increased IgE type 1 and total this serum elevated, eosinophilia in children) (there is a positive
family history of allergic disease)
.environmental factor (Sudden change of air temperature)
.Beta-blocker medications ( propranolol), Cardioselective beta-blockers, ACE inhibitors, aspirin and NSAIDs (Paracetamol
injection) (M.C pharmacological stimulate is ASA, B-blockers, NSAIDs)
.viral and bacterial infections of the upper respiratory tract (M.C stimulate cause asthma is respiratory infections)
.psychological stress
.history of atopic disease (eczema, hay fever)
.dust
.smoking
.paint
.allergens perfumes
-Diagnosis :
.arterial blood gas (is severe asthma decreased Pao2, increased Pco 2 and decreased pH)
.CXR findings are nonspecific in an asthmatic attack (the chest x-ray may be helpful in ruling out acute infection as the cause of
an acute attack)
119
.FEV <80%
-Treatment :
.O2
.bronchodilator (B2 agonist, anticholinergic, aminophylline)
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.corticosteroids IV
.cromolyn sodium
.leukotriene antagonist
+For severe asthma - methylxanthine (aminophylline, theophylline, adrenalin IV)
+B2-agonist
.long acting beta-adrenoceptor agonist (formoterol, salmeterol) – NOT in emergency cases
.short acting beta-adrenoceptor agonist (salbutamol-ventolin, terbutaline) – FOR emergency cases (salbutamol NOT controller)
+Anticholinergic drugs
.long acting (tiotropium)
.short acting (ipratropium bromide)
+Beta-blocker + NSAID (are contraindicated in ASTHMA)
+Severe asthma (peak flow <33% / PaO 2 is high / silent chest / cyanosis / low Bp)
+Acute severe asthma (peak flow 33-50% / respiratory >25 breaths per min. / heart rate >110 / unable to complete sentences in
one brath)
+Signs Of Sever-Life Threatining Asthma :
.inability to complete asentence in one breath
.HR >110 (tachycardia)
.RR >23 (tachypnea)
.silent chest
.Co2 retension (hypercapnia - respiratory acidosis)
.Po2 <60mmHg
.peak flow <33%
+Severity Of Asthma :
.intermittent (FEV1 >80% / Symptoms for <2wks / treated by inhaled cortisone + short acting B 2-agonist as needed)
.mild persistent (FEV1 >80% / Symptoms for >2wks-but not daily / treated by inhaled cortisone + short acting B 2-agonist every
4-6hrs)
.moderate persistent (FEV1 60-80% / Symptoms are daily / treated by inhaled cortisone + short-long acting B 2-agonist)
.severe persistent (FEV1 <60% / Symptoms are throughout day / treated by oral cortisone + short-long acting B 2-agonist)
+Cromolyn sodium / Leukotriene antagonist (zafirlukast – zileuton) – Alternatives for inhaled cortison (decreased frequency of
asthma attack)
++Asthma Medications :
+Rapid Relief Medications (short acting B2 agonist, short acting anticholinergic, systemic cortison - oral or IV)
+Long Term Controller Medications (inhaled cortisone, long acting bronchodilator, cromolyn sodium Na+, leukotriene
antagonist, systemic cortisone)
+Controller Asthma (inhaled cortisone, salmeterol, cromolyn Na +, tiotropium)
+Side Effect Of B2-agonist :
.hypotension
.tachycardia (reflex)
.tremor
.hypokalemia
*Bronchiectasis
-Dilation of bronchi
-Signs & Symptoms :
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.crepitation
.pulmonary hypertension
-Causes :
.post infection (TB, pneumonia, viral infection)
.congenital (cystic fibrosis, kartagener syndrome, immotile cilia syndrome)
.bronchial obstruction (tumor foreign body)
.idiopathic
-Treatment :
.chest physiotherapy
.mucolytics
.antibiotics (M.C bacteria is pseudomonas)
.bronchodilators
+A Large Round Mass In A CXR Might Be Due To :
.Hydatid cyst
.Bronchogenic carcinoma
.Tuberculoma
.Bronchogenic cyst
+The commonest symptom of bronchial carcinoma is Cough
+Pancoast tumor arises in Apex of the lung
+Ranges of hemoglobin saturation in arterial blood is 75-97%
+Regarding CXR :
.Rt. done of diaphragm is seen at the level of 6th anterior rib
.Visceral pleura cover the lung
.Rt. hilum is usually lower than the Lt.
.Pneumothorax appears radiolucent
+Hemoptysis is commonly associated with :
.Bronchiectasis
.Bronchial carcinoma
.Mitral stenosis
.Pulmonary infarction
.Pneumonia
.TB
.Lung trauma
.Goodpasture's syndrome
.Bronchial adenoma
.Aspergilloma
.Pulmonary infarction
.Cystic fibrosis
.Asbestosis
.Bronchitis
.Acute pneumonia
.hypersensitivity pneumonitis
.eosinophilic granuloma
.chronic eosinophilic pneumonia
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.wegener granulomatosis
.idiopathic pulmonary obliterans
.bronchiolitis obliterans
.lymphangioleiomyomatosis
*Sarcoidosis
-Is a disease in which abnormal collections of chronic inflammatory cells (granulomas-Giant cell) form as nodules in multiple
organs / Is a systemic disease of unknown cause, characterized histologically by the presence of nonspecific noncaseating
granulomas in the lung and other organs
+A chronic disease of unknown cause characterized by the enlargement of lymph nodes in many parts of the body and the
widespread appearance of granulomas derived from the reticuloendothelial system
+Sarcoidosis most commonly affected young adults 20-40yrs (disease with a higher prevalence in nonsmokers) / The cause of
sarcoidosis is unknown
+Most often located in the (lungs or the lymph nodes) but any organs can be affected
-Sarcoidosis may be (asymptomatic or chronic) / It commonly improves or clears up spontaneously (asymptomatic Pt., usually in
the form of hilar adenopathy on a CXR)
-Signs & Symptoms :
.may be asymptomatic or chronic
.can affect any organ
.fatigue (unchanged by sleep)
.lack of energy
.weight loss
.aches and pains
.arthritis
.dry eyes
.swelling of the knee
.blurry vision
.shortness of breath
.dry cough
.skin lesions (erythema nodosum or lupus pernio-skin rash or face)
.anemia (occurs in 4-20% of Pts.) , leukopenia (low WBC)
.lymphadenopathy (bilateral hilar lymphadenopathy)
.hypergammaglobulinemia
.hepatosplenomegaly
.hypercalcemia
-Lab Findings :
.hypercalcemia or hypercalciuria (caused by increased circulation of Vit D produced by macrophages)
.elevation in angiotensin-converting enzyme (ACE) – it is nonspecific but can be used follow the course of the disease
.abnormalities in liver function tests
.skin anergy, PFTs may be normal
.uveitis and conjunctivitis are found in >25% of the cases
-Diagnosis :
.Biopsy (non caseating granuloma)
.tuberculin test PPD (negative)
+CxR (changes) are divided into for stages :
.stage 1 (bihilar lymphadenopathy)
.stage 2 (bihilar lymphadenopathy and reticulonodular infiltrates)
.stage 3 (bilateral pulmonary infiltrates)
.stage 4 (fibrocystic sarcoidosis typically with fibrosis - ground glass appearance)
-Treatment :
.corticosteroids (prednisolone) - It should always be treated with steroids
+The disease can remit spontaneously or become chronic, with exacerbations and remissions
+Pts. with sarcoidosis appear to be at significantly increased risk for cancer, in particular lung cancer, malignant lymphomas
+Good prognosis (young, white race, stage 1, erythema nodosum)
+Pad prognosis (old >40yrs, black race, stage IV, lupus pernio, organ involved, cardiac disease)
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*Pneumoconiosis
-Is an occupational lung disease and a restrictive lung disease caused by the inhalation of dust (leads to fibrosis of the lung)
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+A disease of the lungs due to inhalation of dust, characterized by inflammation, coughing, and fibrosis
+Usually appears 20-30yrs after constant exposure to finding agents (metal mining od gold, silver, lead, copper) but can develop
in <10yrs when dust exposure is extremely high (history is of primary importance is assessing possible occupational lung
disease)
-Signs & Symptoms :
.dyspnea
.shortness of breath
.cough + sputum production
.cor pulmonale
.clubbing
.hypoxemia is evident with an increased PAO2-PaO2 gradient
.CXR findings include (small irregular opacities, interstitial densities, ground glass appearance and honeycombing)
+Asbestosis
-Is an occupational lung disease caused by inhalation of asbestos dust
+Silicosis
- Is an occupational lung disease caused by inhalation of silica dust
**Pulmonary Embolism PE
-Is a blockage of the main artery of the lung or one of its branches
-Most commonly results from DVT, and some cases due to the embolization such as (air, fat, amniotic fluid)
+Arise from proximal (above the knee) DVT / Pulmonary embolism can infrequently occur with upper extremity, subclavian and
internal jugular vein thrombosis. This type occurs in Pts. when intravenous catheters are placed in the associated veins. Also in
the pregnant Pt., thrombosis may occur initially in the pelvic ceins rather than follow the usual course of starting in the distal
and then extending to the proximal veins
+Pulmonary embolism and DVT are considered one disease
+When to consider pulmonary embolism and DVTs (High-Risk Pts.) :
.recent surgery (especially orthopedic surgery-knee replacement surgery carries a 70% risk for DVT)
.cancer history (prostate, pelvic, abdominal and breast) (Pts. with unexplained DVT found that 15-20% of these Pts. developed
cancer within the first 2yrs after the diagnosis of a DVT)
.immobile Pts. (hospitalized) / Pts. with significant heart failure / long travel
.acquired thrombophilia
.inheriated thrombophilia
.pregnancy
-Signs & Symptoms :
.shortness of breath-dyspnea (M.C symptom)
.tachypnea (rapid breathing-Co2 is low – respiratory alkalosis)
.tachycardia
.hypoxia
.chest pain (pleuritic)
.hemoptysis
.cough
.pleural effusion
.loud 2nd heart sound (S2)
.raised jugular venous pressure (JVP)
+Signs On ECG :
.sinus tachycardia (M.C sign on ECG)
.Rt. bundle branch block
.Rt. venticular hypertrophy (Rt. axis deviation)
.S1, Q3, T3 (classical)
+Other Symptoms :
.cough (M.C symptom)
.cyanosis
.sudden death
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.pleural effusion
.pleural friction rub
.DVT
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-Complications :
.pulmonary HTN
.Rt. side heart failure (cor pulmonale)
-Diagnosis :
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**Atelectasis
-Is a collapse of part or the entire lung. It is seen most commonly in the immediate postoperative period. It occurs secondary to
poor inspiration or lack of coughing during this time. Mucous plug, tumor or foreign body can also lead to atelectasis
-Signs & Symptoms :
.tachycardia
.dyspnea
.fever
.hypoxemia
.on X-ray, upper lobe atelectasis can appear as tracheal deviation to the affected side
**Pleural Mesothelioma
-M.C malignant tumor of pleura / Most important risk factor is asbestosis
-Signs & Symptoms :
.chest pain
.shortness of breath
.weight loss
.pleural effusion (exudate)
.finger clubbing
-Diagnosis :
.biopsy (pleura)
+prognosis is poor
**Respiratory Failure
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-Types :
1.low po2 / low or normal Pco2
-Causes :
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.pneumonia
.pulmonary embolism
.pulmonary edema
.emphysema
.mild asthma
2.low Po2 / high Pco2
-Causes :
.severe asthma
.chronic bronchitis
.hypoventilation
+The usual causes of low arterial oxygen tension (PaO2) :
.Right to left shunt
.Ventilation perfusion mismatch
.Impaired diffusion capacity
.Hypoventilation
**Hypercapnia
-High Co2
-Signs & Symptoms :
.headache
.vasodilation (warm extremities)
.tachycardia
.tachypnea
.large pulse volume (collapsing pulse)
.tremor (asterixis)
.papilledema
.coma
.altered level of consciousness
**Cystic Fibrosis
-Autosomal recessive disease / Mutation on CFTR gene (chloride channels) or chromosome 7
-Signs & Symptoms :
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+Infants (0-1yr)
.meconium ileus
.failure to thrive
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.rectal prolapse
+Children
.recurrent chest infection
.bronchiectasis
.finger clubbing
.liver cirrhosis
.cyanosis
.gallstones
.nasal polyp
.malabsorption (steatorrhea)
-Diagnosis :
.sweat chloride test >60mmol/L (BEST)
-Treatment :
.chest physiotherapy
.pancreatic enzyme
.supplementation Vit (KEDA)
.antibiotics
.low fat diet
**Lung Infections
*Bronchitis
-Is an infection of the lung, which is limited to the bronchial tree with limited involvement of the lung parenchyma
-Acute Bronchitis is as acute inflammation of the tracheobronchial tube, are caused by (viruses, S.pneumoniae and H.influenza)
have not been implicated (smoking is M.C.C)
-Signs & Symptoms :
.cough often accompanied by sputum production
.a bacterial etiology is suggested by discolored sputum
.Pts. most commonly have clear lungs
.low-grade fever may be present, but Pts. are most commonly afebrile
-Diagnosis :
.signs of respiratory infection such as (cough and sputum, with a normal CXR confirm the diagnosis)
-Treatment :
.mild acute cases often do not require therapy because they are often caused by viruses that resolve spontaneously
.acute exacerbations of chronic bronchitis can be treated with amoxicillin, doxycycline or TMP/SMZ
.repeated infection or Pts. not responding to amoxicillin should be treated with any of the following amoxicillin/clavulanate,
clarithromycin, azithromycin, oral second-or third-generation cephalosporins, or the new fluoroquinolones, gatifloxacin,
levofloxacin or moxifloxacin
*Pneumonia
-Pneumonia is an inflammatory condition of the lung / Rates are greatest in children <5 yrs of age , and adults >75yrs of age
-Signs & Symptoms :
.productive cough
.fever (accompanied by shaking chills)
.shortness of breath
.chest pain during deep breaths (this chest pain worsened by inspiration) (pleuritic pain is associated with lobar pneumonia-
such as pneumococcus)
.increased respiratory rate RR
.high heart rate - tachycardia
.low oxygen saturation
.on physical examination, pneumonia presents with rales, rhonchi or signs of lung consolidation, including dullness to
percussion, bronchial breath sounds, increased vocal fremitus and egophony (E to A changes)
.sputum
.severe pneumonia of any cause may present with dyspnea
+Bacterial infections such as (streptococcus pneumoniae, haemophilus and klebsiella have significant purulent sputum
production)
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+The sputum in Pts. with S.pneumoniae has been classically described as rusty (this rust is simply hemoptysis)
+Klebsiella pneumoniae has been associated with sputum described as being like currant jelly
+Interstitial infections such as those caused by pneumocystis pneumonia (PCP), viruses, mycoplasma and sometimes legionella
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.pulse >125/min
.RR >30/min
.systolic blood pressure <90mm Hg
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.chest tube
.empyema
+Rusty sputum is characteristic of Pneumococcal pneumonia
+Causes Of Aspiration Pneumonia :
.Gastroesophageal reflux
.Achalasia
.Phrenic nerve palsy
.Tracheoesophageal fistula
+Signs Consistent With Lobar Pneumonia :
.Reduced chest movement
.Whispering pectoriloquy
.Pleural rub
.Bronchial breathing
+Viral Pneumonia :
.Amantadine is an effective medication for swine flue
.H1N1 virus is transmitted mainly through milk
.Viral pneumonia is more common than bacterial pneumonia
.Specific radiological findings is characteristic for viral pneumonia
*Lung Abscess
-Necrosis of the pulmonary parenchyma caused by microbial infection
-Signs & Symptoms :
.fever
.cough
.sputum production
.chest pain
.the features associated with lung abscesses are putrid, foul-smelling sputum
.weight loss
.anemia
.fatigue have usually been present prior diagnosis
-Causes :
.90% have at least some anaerobes involved
.the most commonly implicated anaerobes are peptostreptococcus, prevotella and fusobacterium species
.45% only anaerobic, 45% mixed with aerobes, 10% aerobes only
.aerobic bacteria, most frequently involved are S.aureus, E.coli, Klebsiella and Pseudomonas
.pulmonary infarction, cancer and vasculitis (like wegener granulomatosis) are three example of noninfectious causes of lung
cavities
+M.C.C of lung abscess in adults (lung cancer) / In children (foreign body)
+This is probably due to the delay of 1-2 weeks between the aspiration of oral contents and the development of necrosis and
cavitation
-Diagnosis :
.chest CT scan
*Tuberculosis TB
-Is an infectious disease usually caused by the bacterium Mycobacterium tuberculosis (MTB)
+Tuberculosis may infect any part of the body, but most commonly occurs in the lungs (known as pulmonary tuberculosis)
+Airborne transmission (TB is spread through the air)
+Hematogenous transmission can also spread infection to more distant sites, such as (peripheral lymph nodes, the kidneys, the
brain, and the bones)
+Mycobacterium tuberculosis is etiological agent of Pott’s disease
+Active infection occurs more often in people with HIV/AIDS and in those who smoke
+Severe form of TB disease and M.C in young children and those with HIV, is called (Miliary Tuberculosis)
-Signs & Symptoms :
.may infect any part of the body (most commonly occur in the lung)
.chronic cough with blood-containing sputum
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.fever
.chills
.night sweats
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.loss of appetite
.weight loss
.fatigue
.finger clubbing
+Typically found in the top of the lung (in active TB – upper lobe / latent – lower lobe)
-Vaccines :
.Bacillus Calmette-Guerin (BCG) / The immunity is induced decreases after about 10yrs
-Diagnosis :
.CXR (upper low cavitation)
.mantoux tuberculin skin test PPD (previously immunized may have a false positive test)
+>10mm induration (low risk) / >5mm (in high risk)
+PPD is sensitive but NOT specific
.sputum for (ziehl neelsen stain) – TB (acid fast bacilli AFB)
.sputum for culture
+Diagnosis of active TB is based on chest X-rays, as well as microscopic examination and culture of body fluids. Diagnosis of
latent TB relies on the tuberculin skin test (TST) or blood tests
-Treatment :
+Latent TB treatment usually employs a single antibiotic (I.N.H – Isoniazid, rifampicin for 2 months)
+Active TB disease is best treated with combinations of several antibiotics to reduce the risk of the bacteria developing
antibiotic resistance :
.ethambutol (can cause-side effect - optic neuritis)
.isoniazid is INH (can cause - peripheral neuropathy, hepatitis, Vit B6 deficiency ‘pyridoxine’)
.pyrazinamide (can cause – hepatotoxicity, hepatitis)
.rifampicin (can cause - change in the color of all body fluids to orange-red body secretion, red urine, red tears)
+Granulomatous Disease (sarcoidosis – TB)
+Anti TB Drugs :
.Isoniazid (INH)
.Rifampicin
.Pyrazinamide
.Ethambutol
.Streptomycin
.Isonicotinic acid hydrazide (INH)
+Contacts with a patient having TB who recently changed from negative to positive for PPD test should receive INH
+Isoniazid chemoprophylaxis may be given to selected high risk patients over 35yrs of age
+Warfarin
.Oral
.Mechanism (inhibit Vit K dependent, clotting factors II, VII, IX, X (1972), protein)
.Half life 1.5day
.Antidote (Vit K, FFP-plasma)
.Contraindicated in pregnancy (can cause cross placenta)
.PT, INR
+Heparin
.Subcutaneous or I.V
.Mechanism (activated antithrombin III)
.90min-1.5hrs
.Antidote (protamine sulfate)
.safe in pregnancy
.aPTT
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Anaphylaxis, Bites And Stings
**Anaphylaxis
-Syndrome of histaminergic release in which there are signs of severe injury such as urticaria, angioedema, hypotension,
tachycardia and respiratory compromise
-Signs & Symptoms :
.rash known as ‘hives’
.dyspnea
.stridor
.tachycardia
.hypotension
.hemodynamic collapse
-Treatment :
.antihistamine (diphenhydramine)
.for more sever symptoms of anaphylaxis with hemodynamic instability required (epinephrine injections, intravenous fluids,
antihistamines and systemic corticosteroids)
*Human Bites
-The M.C organisms are anaerobic and aerobic bacteria
+Hepatitis B and HIV can also be transmitted through bites bu is much less common
-Treatment :
.clean and irrigate wound
.if bites <12hrs old, close loosely
.give counseling for tetanus, hepatitis B and prophylaxis
.initiate 5-7 days course of prophylaxis antibiotics
*Rabies
-Raccoons, rats, wild dogs, woodchucks, skunks, foxes
-Signs & Symptoms :
.incubation period up to 1yr
.prodrome of 2-10 days including (fever, paresthesias at the bite site)
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.CSF
.serum
-Treatment :
.ribavirin (has been used in confirmed cases)
.prophylaxis with human rabies immunoglobulin (HR16), which gives immediate passive immunity
.human diploid cell vaccine (HDCV) should be given at 0, 3, 7, 14 and 28 days (5 shots total)
*Snake Bites
-Snake venom contains numerous potentially dangerous substances, such as (hemolysis toxic, cardiotoxin, neurotoxin and
proteolytic enzymes. Some of these substances can result in neuromuscular blocked)
-Factors that affect the severity of the bite :
.body size (the smaller the body, the worse the effects)
.location ob bite (trunk and face bites are worse than extremity bites)
.exercising after bite (Muscular activity helps spread the venom through the lymphatics)
.depth of injury (No poisoning occurs in 20-50% of bites because they are too superficial)
-Treatment :
.immobilize the Pt. (this will help to decrease the spread of venom through the lymphatics, which increases with muscular
contraction)
.apply compression bandage (this will decrease lymph flow)
.antivenin
.supportive (hypotension is managed with fluids)
.infective therapy (incision and suction of the bites) (tourniquets and ice immersion do not help and might be harmful)
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NEUROLOGY
**Cerebrovascular Accident CVA (Stroke)
-Is a sudden onset of a focal neurologic deficit, or brain attack (is when poor blood flow to the brain results in cell death) –
Ischemic or Hemorrhagia
-Types :
.Ischemic Strokes (M.C)
.Hemorrhagic Strokes (cerebral hemorrhage, subarachnoid hemorrhage)
.Transient ischemic attacks (TIAs) – Mini strokes (M.C.C is carotid artery stenosis)
-Diagnosis :
.the initial test of choice will always be a non contrast CT scan of the head (this test is done to distinguish between hemorrhagic
and ischemic stroke)
.CT scan is the most sensitive test for detecting blood in the brain
.CT scan are often negative for ischemia within the first 48hrs after symptoms onset
.MRI is the most accurate test for detecting cerebral ischemia
.myoamoya disease
.bacteria (usually from infectious endocarditis)
.cancer cells
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.CHF
.DM
.hyperlipidemia
.homocysteinemia
.smoking
.HTN (M.C.C of intracranial hemorrhage)
.embolism (MI or atrial fibrillation) – Heart disease
.thrombus (carotid artery)
.pulmonary embolism
.pericardial effusion
.hypoxemia
.bleeding
.cerebral venous sinus thrombosis
*Hemorrhagic
-Types :
1. Cerebral hemorrhage or intracerebral hemorrhage (bleeding within the brain itself. Intraparenchymal hemorrhage – bleeding
within the brain tissue Or, Intraventricular hemorrhage – bleeding within the brain`s ventricular system)
2. Subarachnoid hemorrhage (bleeding that occurs outside of the brain tissue but still within the skull, between the arachnoid
mater and pia mater) (associated with polycystic kidney disease) (can cause hyponatremia)
+The blood supply to the brain is divided into tow major systems :
.the carotid (anterior) circulation
.the vertebrobasilar (posterior) circulation
+The major blood vessels comprise the anterior circulation include :
.the anterior cerebral artery ACA
.middle cerebral artery MCA
+Occlusion of the ACA (Anterior Cerebral Artery Stroke) presents with contralateral weakness in the arm and sensory loss in the
leg more than in the upper extremity. Urinary incontinence, confusion and behavioral disturbances are common
+Occlusion of the MCA (Middle Cerebral Artery Stroke) presents with contralateral hemiplegia, hemisensory loss and
homonymous hemianopia with eyes deviated toward the cortical lesion
**Convulsion (FIT)
-is a medical condition where body muscles contract and relax rapidly and repeatedly, resulting in an uncontrolled shaking of
the body
+Because a convulsion is often a symptom of an epileptic seizure, the term convulsion is sometimes used as a synonym for
seizure
+NOT all epileptic seizures lead to convulsions, and not all convulsions are caused by epileptic seizures
-Signs & Symptoms :
.brief blackout
.confusion
.drooling
.loss of bowel/bladder control
.sudden shaking of entire body
.uncontrollable muscle spasms
.temporary cessation of breathing
.symptoms usually last from a few seconds to around 15 minutes
-Causes :
.caused by some sort of electrical activity mishap in the brain
.chemicals in the blood
.infections like meningitis or encephalitis
.fevers
.head trauma
.stroke
.lack of oxygen to the brain
.genetic defects
136
.brain tumors
.by any type-1 diabetic, whose blood sugar is too low. Hypoglycemia can cause very bad convulsions until the person's blood
sugar is raised to normal level
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+The M.C type of seizure is called a generalized seizure, also known as a generalized convulsion. This is characterized by a loss
of consciousness which may lead to the person collapsing. The body stiffens for about a minute and then jerks uncontrollably
for the next minute. During this, the patient may fall and injure themselves or bite their tongue and lose control of their
bladder. A familial history of this puts a person at a greater risk for developing them
**Seizures
-Types :
.Epileptic seizure
.Non-epileptic seizure
-Signs & Symptoms :
.sudden in onset
.with or without an aura
.disorientation
.sleepiness
.aching muscles for minutes to hours after the event
.Pt. may also experience incontinence
.tongue biting
.jerking of a finger or hand
.headache as a result of the seizure
-Causes :
.vascular (stroke, bleed, arteriovenous malformation AVM, cavernoma)
.infection (meningitis, abscess, encephalitis, cerebral malaria, neurocysticercosis)
.trauma (especially penetrating)
.autoimmune (CNS vasculitis)
.metabolic (hyponatremia, hypocalcemia, hypomagnesemia, hypoglycemia, hypoxia)
.idiopathic
.neoplasm (abscesses, tumors)
.psychiatric
.drug overdoses
.drug withdrawal
.drugs (antidepressants, antipsychotics, cocaine, insulin, and the local anaesthetic lidocaine)
.multiple sclerosis
.people with celiac disease also have seizures
+Seizures may occur as a result of high blood pressure, known as hypertensive encephalopathy, or in pregnancy as eclampsia
when accompanied by either seizures or a decreased level of consciousness. Very high body temperatures may also be a cause
+Seizures in a person with a shunt may indicate failure
+Hemorrhagic stroke can occasionally present with seizures, embolic strokes generally do not (though epilepsy is a common
later complication); cerebral venous sinus thrombosis, a rare type of stroke, is more likely to be accompanied by seizures than
other types of stroke
+Head injury may cause non-epileptic post-traumatic seizures or post-traumatic epilepsy
+Difficulties with withdrawal seizures commonly occurs after prolonged alcohol or sedative use, a condition known as delirium
tremens
+In people with brain tumors (the frequency of epilepsy depends on the location of the tumor in the cortical region)
-Diagnosis :
.electroencephalogram is the test of choice fro the diagnosis of epilepsy
.diagnosis of idiopathic seizures is made only after secondary precipitating factors have been ruled out
.an abnormal EEG alone is not diagnostic of epilepsy
.CT scan and MRI of the head is usually indicated to rule out a structural lesion as the cause of seizure
*Epileptic Seizure
-Is a brief episode of signs or symptoms due to abnormal excessive or synchronous neuronal activity in the brain. The outward
effect can vary from uncontrolled jerking movement (tonic-clonic seizure) to as subtle as a momentary loss of awareness
(absence seizure)
+A first seizure generally does not require treatment unless there is a specific problem on either electroencephalogram or brain
imaging
137
+The M.C type of seizures are convulsive (60%). Two-thirds of these begin as focal seizures and become generalized
+Focal Seizures (localized seizures)
.are often preceded by certain experiences, known as an aura sensory, visual, psychic, autonomic, olfactory or motor
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phenomena
.Jerking activity may start in a specific muscle group and spread to surrounding muscle groups—known as a Jacksonian march
.these are known as automatisms and include simple activities like smacking of the lips or more complex activities such as
attempts to pick something up
+Generalized Seizures
.types of generalized seizures (tonic-clonic, tonic, clonic, myoclonic, absence, and atonic seizures)
1.Tonic-clonic seizures present with a contraction of the limbs followed by their extension, along with arching of the back for
10–30 seconds. A cry may be heard due to contraction of the chest muscles. The limbs then begin to shake in unison. After the
shaking has stopped it may take 10–30 minutes for the person to return to normal
2.Tonic seizures produce constant contractions of the muscles. The person may turn blue if breathing is impaired
3.Clonic seizures involve shaking of the limbs in unison
4.Myoclonic seizures involve spasms of muscles in either a few areas or generalized through the body
5.Absence seizures can be subtle, with only a slight turn of the head or eye blinking. The person often does not fall over and
may return to normal right after the seizure ends, though there may also be a period of post-ictal disorientation
6.Atonic seizures involve the loss of muscle activity for greater than one second. This typically occurs bilaterally (on both sides
of the body)
-Duration :
.A seizure can last from a few seconds to more than five minutes, at which point it is known as status epilepticus
.Most tonic-clonic seizures last less than two or three minutes
.Absence seizures are usually around 10 seconds in duration
+Different Causes Of Seizures :
.During the neonatal period and early infancy the most common causes include hypoxic ischemic encephalopathy, central
nervous system (CNS) infections, trauma, congenital CNS abnormalities, and metabolic disorders
.The most frequent cause of seizures in children is febrile seizures, which happen in 2–5% of children between the ages of six
months and five years
.During childhood, well-defined epilepsy syndromes are generally seen
.In adolescence and young adulthood, non-compliance with the medication regimen and sleep deprivation are potential triggers
.Pregnancy and labor and childbirth, and the postpartum, or post-natal period (after birth) can be at-risk times, especially if
there are certain complications like eclampsia.
.During adulthood, the likely causes are alcohol related, strokes, trauma, CNS infections, and brain tumors
.In older adults, cerebrovascular disease is a very common cause. Other causes are CNS tumors, head trauma, and other
degenerative diseases that are common in the older age group, such as dementia
*Non-epileptic Seizure
-Are paroxysmal events that mimic an epileptic seizure but do not involve abnormal, rhythmic discharges of cortical neurons
-Causes :
.Syncope (fainting) (reflex anoxic seizures)
.Breath-holding spells of childhood
.Cataplexy
.Hyperekplexia, also called startle syndrome
.Migraine
.Narcolepsy
.Non-epileptic myoclonus
.Opsoclonus
.Parasomnias, including night terrors
.Paroxysmal kinesigenic dyskinesia
.Repetitive or ritualistic behaviours
.Tics
.AADC Deficiency
*Febrile Seizure
-Is a seizure associated with a high body temperature but without any serious underlying health issue. They most commonly
occur in children between the ages of 6 months and 5 years. Most seizures are less than five minutes in duration and the child is
completely back to normal within sixty minutes of the event
138
.A complex febrile seizure is one in which the seizure lasts longer than 15 minutes or multiple episodes occur within 24 hours
and generally does have focal features
.A febrile status epilepticus is a febrile seizure that lasts for longer than 30 minutes. It can occur in up to 5% of febrile seizure
cases
+Febrile seizures may run in families
+The diagnosis involves verifying that there is not an infection of the brain, there are no metabolic problems, and there have
not been prior seizures that have occurred without a fever
+Febrile seizures without an intracranial infection or metabolic problems. They run in families. Several genetic associations have
been identified. An association with iron deficiency has also been reported, particularly in the developing world
*Epilepsy
-Is a group of neurological diseases characterized by epileptic seizures
+Epilepsy is characterized by a long-term risk of recurrent seizures. These seizures may present in several ways depending on
the part of the brain involved and the person's age
-Causes :
.broken bones
.brain-head injury
.toxic ingestion or metabolic problem
.stroke
.brain tumors
.infections of the brain (cerebral malaria, toxoplasmosis, toxocariasis)
.infections of CNS
.birth defects
.cerebral cavernous malformations
.arteriovenous malformations
.chronic alcohol use
.meningitis, herpes simplex encephalitis, pork tapeworm, neurocysticercosis
.genetic mutations (ion channels, enzymes, GABA, and G protein-coupled receptors, Down syndrome, Angelman syndrome)
.excessive and abnormal nerve cell activity in the cortex of the brain
.more common in among younger people
.malnutrition
.cerebral palsy
.spastic quadriplegia – spastic hemiplegia
.alzheimers disease, multiple sclerosis, tuberous sclerosis, autoimmune encephalitis
+Getting vaccinated does not increase the risk of epilepsy
*Syncope
-Treatment :
139
+Returning blood to the brain by positioning the person on the ground, with legs slightly elevated or leaning forward and the
head between the knees for at least 10–15 minutes, preferably in a cool and quiet place
.Beta blockers (β-adrenergic antagonists)
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.Medications which may be effective include: CNS stimulants fludrocortisone, midodrine, SSRIs such as paroxetine or sertraline,
disopyramide, and, in health-care settings where a syncope is anticipated, atropine epinephrine (adrenaline)
+Vasovagal Syncope (M.C type)
-Is a malaise mediated by the vagus nerve and it leads to fainting. Is most commonly found in adolescents and in younger adults
-Signs & Symptoms :
.bradycardia
.emotion (fear, pain)
+Pt. with syncope (they will recover consciousness within several minutes of the event, and no physical exam will not have
evidence of incontinence or tongue biting)
-Causes :
.Prolonged standing (standing too long) or upright sitting
.Hypoglycemia
.Anxiety (hyperventilation)
.Factitious syncope (temporary loss of consciousness caused by a fall in blood pressure)
.After or during urination (micturition syncope)
.Standing up very quickly (orthostatic hypotension)
.During or post-biopsy procedures.
.Stress directly related to trauma[8]
.Stress
.Postural orthostatic tachycardia syndrome (POTS)
.Any painful or unpleasant stimuli, such as (rauma - such as hitting one's funny bone, watching or experiencing medical
procedures - such as venipuncture or injection, high pressure on or around the chest area after heavy exercise)
.Severe menstrual cramps
.Sensitivity to pain
.Arousal or stimulants, e.g. sex, tickling, or adrenaline
.Sudden onset of extreme emotions
.Lack of sleep
.Dehydration
.Hunger
.Being exposed to high temperatures
.In health care, such as nursing care
.Use of certain drugs that affect blood pressure, such as cocaine, alcohol, marijuana, inhalants, and opiates
.The sight of blood
.Serotonin level / SSRI
.Swallowing
+Exertional Syncope
-Syncope with exercise, causes (aortic stenosis, hypertrophic cardiomyopathy)
**Dizziness
-Is an impairment in spatial perception and stability or loss of consciousness indicates a concussion has occurred
+Is defined as afalse sensation of mevement, i.e, the sensation of mevement in the absence of actual movement
-Classification :
.vertigo (~50%)
.disequilibrium (less than ~15%)
.presyncope (less than ~15%)
.lightheadedness (~10%)
+Vertigo is the sensation of spinning or having one's surroundings spin about them. Many people find vertigo very disturbing
and often report associated nausea and vomiting
.Pts. who experience vertigo will describe a sensation of movement without actually moving (Pts. will describe their
environment spinning around them). Sensation of tiling, swaying, or falling forward or backward are all consistent with vertigo.
These episodes are commonly associated with nausea and vomiting (tinnitus, hearing loss present in peripheral vertigo /
peripheral vertigo treated by meclizine or, in severe cases, diazepam – absent in central vertigo)
+Disequilibrium is the sensation of being off balance, and is most often characterized by frequent falls in a specific direction.
This condition is not often associated with nausea or vomiting
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+Presyncope is Lightheadedness, muscular weakness and feeling faint as opposed to a syncope, which is actually fainting
.Pts. who complain of presyncope will describe their symptoms as ‘lightheadedness’ or ‘feeling like im going to back out’,
weakness, palpitations and shortness of breath
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+It is essential to differentiate vertigo from presyncope because vertigo is usually a manifestation of neurologic disease,
whereas presyncope is a cardinal manifestation of cardiovascular disease
-Causes :
.benign paroxysmal positional vertigo
.traumatic vertigo
.cervical vertigo
.perilymphatic fistula
.vascular disease of the brainstem
.arteriovenous malformations
.drug overdose
.meniere's disease
.vestibular neuronitis
.labyrinthitis
.otitis media
.brain tumor
.acoustic neuroma
.motion sickness
.ramsay Hunt syndrome
.migraine
.multiple sclerosis
.pregnancy
.low blood pressure (hypotension)
.low blood oxygen content (hypoxemia)
.heart attack
.iron deficiency (anemia)
.low blood sugar (hypoglycemia)
.hormonal changes (e.g. thyroid disease, menstruation, pregnancy)
.panic disorder
.hyperventilation
.anxiety
.depression
.age-diminished visual, balance, and perception of spatial orientation abilities
+A stroke is the cause of isolated dizziness in 0.7% of people who present to the emergency room
+Non-specific dizziness is often psychiatric in origin. It is a diagnosis of exclusion and can sometimes be brought about by
hyperventilation
+Many conditions cause dizziness because multiple parts of the body are required for maintaining balance including the inner
ear, eyes, muscles, skeleton, and the nervous system
+Physiological Causes Of Dizziness :
.inadequate blood supply to the brain due to (a sudden fall in blood pressure) (heart problems or artery blockages)
.loss or distortion of vision or visual cues
.disorders of the inner ear
.distortion of brain/nervous function by medications such as anticonvulsants and sedatives
.result of side effect from prescription drugs, including proton-pump inhibitor drugs (PPIs) and Coumadin (warfarin) causing
dizziness/fainting
+Ménière's Disease
-Is a disorder of the inner ear that can affect hearing and balance. It is characterized by episodes of vertigo, tinnitus, and
hearing loss. The hearing loss comes and goes for some time, alternating between ears, then becomes permanent
-Signs & Symptoms :
.nausea, vomiting
.sweating
.unilateral (in one ear) or bilateral (both ears) hearing loss
.unilateral or bilateral tinnitus
.unilateral or bilateral sensation of fullness or pressure
.uncontrollable rhythmical and jerky eye movements
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.migraine
+Other conditions can present themselves with Ménière's-like symptoms, such as (syphilis, Cogan's syndrome, autoimmune
inner ear disease, dysautonomia, perilymph fistula, multiple sclerosis, acoustic neuroma, and both hypo- and hyperthyroidism)
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-Causes :
.Menière's disease is linked to endolymphatic hydrops
.membranous labyrinth
.related to swelling of the endolymphatic sac or other tissues in the vestibular system of the inner ear
.middle ear infection
.head trauma
.upper respiratory tract infection
.from using aspirin
.smoking cigarettes, or drinking alcohol
.HSV
+Is treated with low-salt diet and diuretics (in Pts. who fail medical therapy, you can consider surgical decompression)
+Labyrinthitis (otitis interna)
-Is inflammation of the inner ear. It results in vertigo and also possible hearing loss or ringing in the ears. It can occur as a single
attack, a series of attacks, or a persistent condition that diminishes over three to six weeks. It may be associated with nausea,
vomiting. Vestibular neuronitis may also be associated with eye nystagmus
.present with sudden onset of severe vertigo that lasts for several days with hearing loss and tinnitus. The disease frequently
follows an upper respiratory tract infection
+Is treated symptomatically with meclizine and diazepam when the symptoms are severe (vertigo seconadry to labyrinthitis)
*Tremor
-Causes :
.multiple sclerosis
.stroke
.familial (relieved alcohol)
.hyperthyroidism
.traumatic brain injury
.chronic kidney disease
.neurodegenerative diseases (that damage or destroy parts of the brainstem or the cerebellum)
.parkinson's disease
.drugs (such as amphetamines, cocaine, caffeine, corticosteroids, SSRIs, B 2-agonist-salbutamol) or alcohol, mercury poisoning
.withdrawal of drugs such as alcohol or benzodiazepine
.in infants with phenylketonuria (PKU), overactive thyroid or liver failure
.hypoglycemia
.lack of sleep, anxiety, lack of vitamins, or increased stress
.deficiencies of magnesium and thiamine
.spider bites (the redback spider)
.rhythmic shaking in the hands, arms, head, legs, or trunk; shaky voice; and problems holding things such as a fork or pen
-Clinical Presentation :
.A history of recurrent symptoms makes the diagnosis of a primary headache disorder more likely
.headache with fever and nuchal rigidity suggests meningitis as the underlying cause
.accompanied by nuchal rigidity without fever, suggests as intracranial hemorrhage is the underlying cause
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.Pts. with brain tumors will present complaining of headache that is described as a deep, dull, aching pain that disturbs sleep
.the history of vomiting that precedes the onset of headache by a number of weeks, or a history of headache induced by
coughing, lifting or bending, is a typical of posterior fossa brain tumors
.Pts. with temporal arteritis complain of a unilateral pounding headache associated with visual changes, described as dull and
boring with superimposed lancinating pain. Pts. will also complain of polymyalgia rheumatica, jaw claudication, fever, weight
loss and scalp tenderness (difficulty combing hair or lying on a pillow). The scalp tenderness is from pain over the temporal
artery
.temporal arteritis is a disorder of the elderly, generally presenting in Pts. older than 50yrs of age. Temporal arteritis gives an
elecated sedimentation rate and is diagnosed with biopsy of the temporal artery. Do not wait for the biopsy results to initiate
therapy with steroids
.Pts. with glaucoma will usually give a history of eye pain preceding the onset of the headachemn
-Diagnosis :
.Pts with severe, sudden onset of a first-time headache accompanied by strong evidence for an underlying cause on history or
physical examination should have a CT scan of the rule out any secondary cause
-Treatment :
.mild migraine (wich is defined as headache in the absence of nausea or vomiting – nonsteroidal anti-inflammatory
medications)
.the triptans are contraindicated in Pts with known cardio-vascular disease
.prophylactic treatment for migraine therapy should be initiated when Pts have acute migraine headache more than 3-4 times
per month (propranolol, timolol, valproic acid and topiramate)
+MIGRAINE THERAPIES :
.abortive (NSAIDs, aspirin, acetaminophen / triptans / ergotamine derivatives)
.prophylactic (beta blockers, calcium blockers, tricyclics, SSRIs, valproic acid, topiramate)
+Migraine Headaches
.F > M 2:1 (More in obese)
.are defined as a benign and recurrent syndrome of headache, nausea, vomiting and other varying neurologic dysfunction
.UNILATERAL headache (Attack lasr 4-72hrs)
.Pts. will describe the headache as pulsatile, throbbing, unilateral and aggravated by minor movement. Other associated
features include photophobia, phonophobia, nausea, vomiting and the time to maximal pain 4-72hrs
.typical triggers (triggers can be identified) include (alcohol, certain foods such as chocolate, various cheeses, monosodium
glutamate), hunger or irregular sleep patterns
.migraine without aura is a migraine without a preceding focal neurologic deficit
.migraine with aura (classic migraine) is a migraine headache that is accompanied by a preceding aura that consists of motor,
sensory or visual symptoms
.risk factors (cheese, OCP, travel, excercise)
.treated by (NSAIDs – aspirin, ketoprofen) / prophylaxis (if >2 attack per month) / B-blocker (propranolol) is decreased
frequency of attacks
+Tension Headache
.M.C type of headache
.BILATERAL headache
.described as tight, ‘band-like’ headache
.Pts. may also describe their headache as ‘vise-like’, and these headaches may be associated with tightness of the posterior
neck muscles / NO vomiting
.relieved by simple analgesic (paracetamol)
.movement will not generally exacerbate the headache
+Cluster Headache
.begin without warning and are typically described as excruciating, periorbital and peaking in intensity within 5min of onset
.UNILATERAL (around one eye)
.the attacks will last from 30min-3hrs and occur one to three times a day for a 4-8wks period
.symptoms associated with cluster headache include (rhinorrhea, reddening of the eye, lacrimation, nasal stuffiness, nausea
and sensitivity to alcohol)
.food and emotion rarely will trigger a cluster headache
.prophylaxis (verapamil-INN)
143
*Pseudotumor Cerebri (Idiopathic intracranial hypertension IIH / Benign intracranial hypertension BIH)
-Is an idiopathic increase in intracranial pressure also known as benign intracranial hypertension (can cause headache). The
disorder is 8-10 times more common in women (F > M)
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+Is a neurological disorder that is characterized by increased intracranial pressure (pressure around the brain) in the absence of
a tumor or other diseases
+Respiratory irregularities, HTN, Bradycardia
-There is association with (epilepsy, brain masses, intracranial bleeding, obesity, chronic lung disease, addison disease, oral
contraceptive, long-term tetracycline use and Vit A toxicity)
-Signs & Symptoms :
.headache
.visual disturbances such as (diplopia, sixth cranial nerve ‘abducens’ palsy)
.papilledema
.enlargement of the blind spot on visual field testing
.worse in the morning
.associated with nausea and vomiting
.the pain may also be experienced in the neck and shoulders
.pulsatile tinnitus
.compression and traction of the cranial nerves, a group of nerves that arise from the brain stem and supply the face and neck
.papilledema (which is swelling of the optic disc, the spot where the optic nerve enters the eyeball)
.visual fields
+Most commonly, the abducens nerve (sixth nerve - This nerve supplies the muscle that pulls the eye outward) is involved
+The headache can be made worse by any activity that further increases the intracranial pressure, such as coughing and
sneezing
+Lumbar puncture is performed to measure the opening pressure, as well as to obtain cerebrospinal fluid (CSF) to exclude
alternative diagnosis / as a diagnostic LP (such as done in search of a CSF infection) (is contraindicated when pressure is
increased)
-Treatment :
.weight loss, removing offending agents such as oral contraceptive
.use of diuretics (acetazolamide or furosemide)
.steroids (prednisone) (used in severe papilledema – otherwise their use is controversial)
.repeated lumbar punctures may help (to exclude diagnosis)
.if this not effective and the disorder does not resolve, definitive treatment can be achieved with the placement of a surgical
shunt between the ventricles and the peritoneum)
+Acetazolamide (Diamox), which acts by inhibiting the enzyme carbonic anhydrase, and it reduces CSF production by six to 57
percent. It can cause the symptoms of hypokalemia (low blood potassium levels), which include muscle weakness and tingling
in the fingers. Acetazolamide cannot be used in pregnancy, since it has been shown to cause embryonic abnormalities in animal
studies. Also, in human beings it has been shown to cause metabolic acidosis as well as disruptions in the blood electrolyte
levels of newborn babies
+One, two, or all three branches of the nerve may be affected. Trigeminal neuralgia most commonly involves the middle branch
(the maxillary nerve or V2) and lower branch (mandibular nerve or V3) of the trigeminal nerve
-Treatment :
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**Multiple Sclerosis MS
-Is an autoimmune inflammatory disease of the CNS white matter characterized by a relapsing or progressive course
+Is an inflammatory disease in which the fatty myelin sheaths around the axons of the brain and spinal cord are damaged,
leading to demyelination and scarring as well as a broad spectrum of signs and symptoms
+Disease onset usually occurs in young adults (F > M) / MS being much less common in people living near the equator
+In MS, the body's own immune system attacks and damages the myelin particularly in the white matter of the brain and spinal
cord
+The Types Of MS :
.relapsing (remitting) (good)
.progressive (worst)
+The Three Main Characteristics Of MS Are :
.the formation of lesions in the central nervous system (also called plaques)
.inflammation
.the destruction of myelin sheaths of neurons
-Signs & Symptoms :
.muscle weakness
.muscle spasms
.clonus
.difficulty in moving
.numbness, tingling
.Lhermitte's sign (electrical sensation that runs down the back when bending the neck)
.difficulties with coordination and balance (ataxia)
.problems in speech (dysarthria)
.dysphagia
.unsteadiness of a limb
.fatigue, acute or chronic pain
.bladder and bowel difficulties (urinary-stool incontinence, urgency or retention)
.visual problems (blurry - double vision, nystagmus, optic neuritis, transient loss of vision-amaurosis fungus)
.emotional symptoms (depression, unstable mood)
.paraplegia, paresthesia
+M.C affect spinal cord (Cervical)
+Rarely affect PNS (bad prognosis)
+Associated Conditions (Lhermitte's sign) :
.the cervical cord or of the caudal medulla
.transverse myelitis
.Behçet's disease
.trauma
.radiation myelopathy
.vitamin B12 deficiency (subacute combined degeneration)
.compression of the spinal cord in the neck from any cause such as (cervical spondylosis, disc herniation, tumor, and Arnold-
Chiari malformation)
.chemotherapy
+Symptoms may persist for several weeks or may resolve spontaneously over a few days
+Most Pts. will have a months-long to years-long disease-free period after their first exacerbation
+In some Pts. the progression of disease becomes more aggressive, so that a consistent worsening of function occurs (this form
of the disease is called secondary progressive disease)
+The diagnosis is made clinically when a young Pt. (usually less than 55yrs of age) presents with a history of multiple neurologic
complaints that cannot be explained by the presence of one CNS lesion (in other words, you should suspect the diagnosis when
a Pt. present with multiple neurologic deficits separated by time and space-anatomy)
+A number of triggers are known to exacerbate the disease. Infections or trauma may acutely worsen the disease. Pregnancy,
especially the 2-3 months following birth
-Causes :
145
+Is unknown; however, it is believed to occur as a result of some combination of genetic and environmental factors such as
infectious agents
+MS is not considered a hereditary disease / The cause of MS is thought to be multifactorial
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.specific genes that have been linked with MS include differences in the human leukocyte antigen (HLA) system (a group of
genes on chromosome 6 that serves as the major histocompatibility complex - MHC)
+The association between multiple sclerosis and alleles of the MHC defined as DR15 and DQ6. Other loci have shown a
protective effect, such as HLA-C554 and HLA-DRB1*11
.infectious agents (hygiene hypothesis, HSV, ep virus, MMR)
.smoking, stress
.gout (low levels of uric acid)
.inflammation (the inflammatory process is caused by T cells, a kind of lymphocyte that plays an important role in the body's
defenses)
.the blood–brain barrier (is a part of the capillary system that prevents the entry of T cells into the central nervous system)
-Diagnosis :
.MRI (of the brain is the most accurate test to diagnose MS)
.McDonald criteria
.cerebrospinal fluid CSF analysis (by LP – high IgG) usually reveals a mild pleocytosis (usually less than 50 cells/ML), and total
protein that is mildly elevated (100mg/dL)
-Treatment :
.cortisone
.interferon-B1b and mitoxantrone (decreased frequency of attack)
+Good Prognosis (relapsing-remitting, female, optic neuritis, sensory symptoms-paresthesia, feq attacks, early age of onset-
younger)
+Pad Prognosis (male, progressive, spinal cord-paraplegia, diabetic, old age)
**Parkinson's Disease
-The motor symptoms of Parkinson's Disease result from the death of dopamine-generating cells in the substantia nigra, a nigra,
a region of the midbrain (Basal Ganglia) / Is a degenerative disorder of the central nervous system mainly affecting the motor
system
-Classifications :
1.primary or idiopathic
2.secondary or acquired
3.hereditary parkinsonism, and
4.Parkinson plus syndromes or multiple system degeneration
-Signs & Symptoms :
.movement-related (these include shaking, rigidity, slowness of movement and difficulty with walking and gait)
.later, thinking and behavioral problems may arise, with dementia commonly occurring in the advanced stages of the disease,
and depression being the most common psychiatric symptom. Other symptoms include sensory, sleep, and emotional problems
.tremor (pill rolling tremor) (rest tremor) – disappearing with voluntary movement and sleep
.bradykinesia - hypokinesia (Slowness of movement)
.rigidity (hypertonia – is stiffness and resistance to limb movement caused by increased muscle tone)
.lead-pipe rigidity and cogwheel rigidity
.mask-like face expression or small handwriting
.voice disorders (speech and swallowing disturbances)
.rapid shuffling steps and a forward-flexed posture
+Dementia (is late symptom)
-Causes :
.idiopathic
.drugs (neuroleptic agents-haloperidol, chlorpromazine / antiemetics-metoclopramide / alpha methyldopa / reserpine)
.poisoning from MPTP
.carbon monoxide
.cyanide
.structural lesion around the basal ganglia (trauma, tumor, abscess ,infarct)
+Parkinson + syndromes :
.parkinsonism + vertical gaze palsy = supranuclear palsy
.parkinsonism + prominent ataxia = olivopontocerebellar atrophy
.parkinsonism + prominent orthostatic hypotension = shy-Drager syndrome
-Diagnosis :
146
-Treatment :
.dopamin - metabolite (treatment to decreased symptoms) (Monoamine oxidase B – MoaB)
+Upper Motor (hyper-reflexia, hypertonia, rigidity, NO atrophy, clonus, babinski sign +)
+Lower Motor (hyporeflexia, hypotonia-atonia, flaccid, atrophy of muscles, fasciculation, fibrillation)
+Poor Prognosis (age over 40yrs, history of preceding diarrheal illness, requiring ventilator support, high anti-GM1 titre, poor
upper-limb muscle strength)
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**Myasthenia Gravis MG
-Is an autoimmune neuromuscular disease leading to fluctuating muscle weakness and fatigability / young Pt.<40 yrs
+Antibodies that block acetylcholine receptors at the postsynaptic neuromuscular junction
+About 10% of MG Pts. are found to have tumors in their thymus glands (thymoma - benign tumor)
-Signs & Symptoms :
.fatigability
.muscles become progressively weaker during periods of activity and improve after periods of rest
.weakness of the eye muscles (M.C) (ptosis)
.dysphagia
.dysarthria
.asymmetrical ptosis (a drooping of one or both eyelids), diplopia (double vision)
.myasthenic crisis a paralysis of the respiratory muscles occurs, necessitating assisted ventilation
+Crises may be triggered by (infection, fever, an adverse reaction to medication, or emotional stress)
+Reflexes and Feeling (sensation( are normal
+Since the heart muscle is only regulated by the (autonomic nervous system). It is generally Unaffected by MG
-Diagnosis :
.electromyography EMG (BEST and most sensitive(
.CT (for thymoma)
-Treatment :
.acetylcholinesterase inhibitors (neostigmine and pyridostigmine)
.immunosuppressive drugs (prednisone, cyclosporine, mycophenolate mofetil and azathioprine)
.plasmapheresis or IVIG (for emergency treatment)
.thymectomy (is a surgical method to treat MG)
+MG (young <40yrs, antibody against nicotinic receptor, fatigability, eye muscle commonly affect, reflexes and sensation are
normal, associated with thymoma)
+2
+LEMS (old >40yrs, antibody against Ca channels-presynaptic, NO fatigability, rarely affect eye muscle, hyporeflexia,
associated with small cell lung cancer)
**Dementia
-Is a serious of global cognitive ability in a previously impaired person, beyond what might be expected from normal aging
+Alzheimer's Disease is still the most frequent cause
+Is far more common in the geriatric population, it can occur before the age of 65 yrs, in which case it is termed “early onset
dementia”
+Affected areas of cognition may be memory, attention, language and problem solving
+It is normally required to be present for at least 6 months to be diagnosed
+Delirium can be easily confused with dementia due to similar symptoms
+In Comparison :
.Delirium is characterized by a rapid-sudden onset, fluctuating course, a short duration (often lasting from hrs to wks)
.Dementia is characterized by a slow-gradual onset, NOT fluctuating course, as well as a progressive-longer duration (from
months to yrs) (slow decline of mental functioning)
148
-Causes :
+Irreversible (90%) / Reversible (10%)
.Alzheimer's Disease (M.C.C)
.vascular dementia
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-Diagnosis :
.Mini-mental state examination
**Alzheimer's Disease AD
-It is a chronic neurodegenerative disease that usually starts slowly and gets worse over time. The most common early
symptom is difficulty in remembering recent events (short-term memory loss)
-Signs & Symptoms :
.problems with language
.disorientation (including easily getting lost)
.mood swings
.loss of motivation
.not managing self care
.behavioural issues
-Causes :
.unknown
.amyloid hypothesis postulates that abeta-amyloid (beta A) deposits are the fundamental cause
+Support for this postulate comes from the location of the gene for the amyloid precursor protein APP on chromosome 21
+People with trisomy 21 (Down Syndrome) who have an extra gene copy almost universally exhibit AD by 40yrs of age
-Characteristics :
+Early
.impairment of learning and memory
.older memories of the person`s life are affected to a lesser degree than new facts or memories
+Moderate
.unable to perform most common activities of daily living
.speech difficulties (inability to recall vocabulary)
+Advanced
.completely dependent upon caregivers
.language is reduced to simple phrases or even single words, leading to complete loss of speech
.aggression and psychosis
-Treatment :
.acetylcholinesterase inhibitors (tacrine, rivastigmine, galantamine and donepezil)
+Life expectancy of the population with the disease is reduced / The mean life expectancy following diagnosis is approximately
seven years
Infectious Diseases
**Central Nervous System Infections
*Meningitis
-Is inflammation of the protective membranes covering the brain and spinal cord, known collectively as meninges
+The inflammation may be caused by infection with (Viruses – Aseptic) (Bacteria – Septic)
+Most cases of meningitis arise sporadically
-Signs & Symptoms :
.headache
.neck stiffness (increased neck muscle tone)
.fever (sudden)
.confusion or altered consciousness
.photophobia (inability to tolerate light) or phonophobia (loud noises)
.nuchal rigidity (neck stiffness, positive kernig's and brudzinski's signs) – Occurs in 70% of bacterial meningitis in adults
.nausea, vomiting
.altered mental status (is possible as well and can make a Pt. seem like they have encephalitis)
+Small children often exhibit only nonspecific symptoms, such as (irritability, drowsiness, decreased activity and feeding, look
unwell, seizure)
.any form of CNS infection can present with seizures
.focal neurologic deficits (M.C being visual field and cranial nerve deficits)
.the M.C long-term neurologic deficit from bacterial meningitis is damage to the 8 th cranial nerve
+If a rash is present, it may indicate a particular cause of meningitis; for instance, meningitis caused by meningococcal bacteria
.rash is associated with several different types of meningitis (A petechial rash is suggestive of neisseria) (A rash on the wrists
and ankles with centripetal spread toward the body is suggestive of RMSF) (Facial nerve palsy is suggestive of lyme disease)
(Pulmonary symptoms or an abnormal CXR suggest TB)
-Causes :
.Streptococcus Pneumoniae is the M.C.C for all Pts. beyond the neonatal period in the past (Haemophilus influenza type B in
countries that do not offer vaccination)
.Neisseria Meningitidis (meningococcus) is spread by respiratory droplets and is the M.C.C of meningitis in adolescents (Older
children)
.Listeria Monocytogenes is more common in those with immune system defects, particulary of the cellular (T-cell) immune
system and sometimes neutrophil defects. These defects include (HIV, steroid use, leukemia, lymphoma and virous
chemotherapeutric agents)
.Staphylococcus Aureus is more common in those who have had any form of neurosurgery (because instrumentation and
damage to the skin introduce the organism into the CNS)
.Cryptococcus is more common in those who are HIV positive and who have profound decreases in their T-cell counts to levels
less than 100 cells
.Group B Streptococci (Streptococcus agalactiae) is the M.C.C of meningitis in the neonatal period (Premature babies and
newborns up to 3 months)
.Tuberculous Meningitis, which is meningitis caused by (Mycobacterium tuberculosis) (Is more common in people from
countries where TB is endemic, but is also encountered in persons with immune problems, such as AIDS)
+Viruses Causing Meningitis Include (enteroviruses, arboviruses ‘St.louis encephalitis virus, West nile virus’, HIV, herpes
simplex and lymphocytic choriomeningitis virus)
+Local Infections That Can Lead To Meningitis Include (otitis media, sinusitis, mastoiditis and dental infections). Hematogenous
spread could possibly occur from any infection but is more common with endocarditis and pneumonia
150
+Neonates and the elderly have decreased T-cell immune function; therefore, listeria is more common in the very young and
the very old. (however, it is critical to remember that evet with immune deficits, Streptococcus pneumoniae is still the M.C.C-it
is just that listeria is more common in these Pts, as compared to fully immunocompetent Pts.)
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-Complications :
.sepsis
.low or abnormally low temperature (Hypothermia <35)
.rapid breathing
.falling blood pressure
.fast heart rate
.DiC
.hemorrhage of the adrenal glands (leading to Waterhouse-Friderichsen Syndrome) (Meningococcal)
.seizures
.abnormalities of the cranial nerves
.visual symptoms and hearing loss (To reduce complications of neurological disorders – Dexamethasone)
-Diagnosis :
.lumbar puncture is essential for establishing the diagnosis (CSF)
.CT scan of the head is the best initial diagnostic test if the Pt. has papilledema, focal motor deficits, new onset seizures, or
severe abnormalities in mental status, or is immunocompromised (HIV infection, immunosuppressive medications, post-
transplantation)
+CSF Findings In Different Forms Of Meningitis :
.Bacteria (Glucose – low / Protein – high / Cells – high PMN >300) (High pressure) (WBC – neutrophil)
.Virus (Glucose – normal / Protein – normal or high / Cells – mononuclear <300) (Normal pressure) (WBC – lymphocyte)
.Tuberculous (Glucose – low / Protein – high / Cells – mononuclear and PMN <300)
.Fungal (Glucose – low / Protein – high / Cells - <300)
.Malignant (Glucose – low / Protein – high / Cells – usually mononuclear)
+Gram staining of the sample may demonstrate bacteria in bacterial meningitis, but absence of bacteria does not exclude
bacterial meningitis as they are only seen in 60% of cases
+If non of the above is present, a lumber puncture can be safely done without doing a CT scan of the head first
+If the lumber puncture is delayed more than 20-30 mins for any reason, then the best initial step is to give as empiric dose of
antibiotics
+The most accurate test for bacterial meningitis on the lumber puncture is the culture of the CSF
+Pneumococcal – Contagious / Meningococcal – NOT
+Specific Diagnosis Of Non-bacterial Meningitis (is based on the nature of the organism) :
.lyme disease and RMSF are best detected with a specific immunological response and cytology
.cryptococcus neoformans is detected initially with an india ink test and then later with an elevation in the serum and CSF
cryptococcal antigen titer
.syphilis is confirmed by the presence of a positive VDRL or FTA on CSF
.TB is rarely detected by AFB smear
.culture for TB has a much higher yield, PCR can also aid in the diagnosis of TB
-Treatment :
.bacterial meningitis in adults is best achieved with (vancomycin)
+Vancomycin is used if you have definite or suspected pneumococcal resistance to penicillin or if there is a chance of
staphylococcal infection after neurosurgery
.ampicillin is added to those with immune defects to cover listeria and for Pts. over 50 yrs of age or <1 months old
.lyme disease is best treated with ceftriaxone
.cryptococcosis is treated with amphotericin
+Prophylactic (rifampin, ciprofloxacin or ceftriaxone)
+The M.C route of infection of most types of meningitis is the blood stream
+Post Traumatic Meningitis :
.Occurs within 2 weeks in most of the cases
.Most of the cases are associated with base skull fracture
.Antibiotics is the main line of treatment
.CSF fistula should be treated if present
.The most common organism in post traumatic meningitis is Pneumococcal
+A 15 months old child developed hydrocephalus following meningitis. The most likely causative organism is H.influenza
+The most common organism causing meningitis in toddlers (6 months - 3 years) is Haemophilus influenzae type B
+Incubation period meningococcal meningitis is usually 2-3 days
+Refusal of feeding is the earliest sign in a newborn with sepsis and meningitis
151
*Encephalitis
-Is an infection of the brain. This includes both the meninges, as well as the brain parenchyma
-Signs & Symptoms :
.fever and headache occur (nonspecific)
.altered mental status with fever and headache is the primary clue to the diagnosis
.any level of neurologic deficit may occur, ranging from slight confusion to lethargy or coma
.focal deficits of any kind can occur
.neck stiffness similar to that found in meningitis can occur (making it difficult to distinguish encephalitis from meningitis)
.seizures
-Causes :
.any bacterial, protozoal or rickettsial infection (the majority is caused by viruses)
.any virus can cause encephalitis, the M.C.C is herpes simplex, usually type-1 (HSV-1)
.varicella-zoster virus, CMV, enterocolitis, eastern and western equine encephalitis, ST.louis encephalitis, and west nile
encephalitis can also occur but are much less common than HSV
-Diagnosis :
.CT or MRI scan of the head should be performed
.for HSV (LP + PCR)
-Treatment :
.HSV encephalitis is best treated with intravenous acyclovir (famciclovir and valacyclovir have activity against HSV, they are not
available intravenously) (ganciclovir or foscarnet are active against CMV)
*Brain Abscess
-A collection of infected material within the brain parenchyma
-Signs & Symptoms :
.headache is the M.C symptom
.fever can be present
.focal neurologic deficits are the initial complaint in about 60% of Pts
.seizures may occur (as with any form of anatomic abnormality of the CNS) (all CNS infections can cause seizures)
-Causes :
.bacteria can spread into the brain from contiguous infections such as (otitis media, sinusitis, mastoiditis or dental infections)
.organisms may also spread through the bloodstream from endocarditis or pneumonia and seed the brain
.toxoplasmosis (can reactive in those with severe HIV disease when their CD4 counts are very low <50-100/mL)
.brain abscesses most commonly have (Streptococcus in 60-70%, bacteroides in 20-40%, enterobacteriaceae in 25-35% and
staphylococcus in 10% and are often polymicrobial)
-Diagnosis :
.the initial test is the CT scan
.MRI is even more accurate than is the CT scan
.no radiologic test alone can give the precise etiology (in the case of bacterial brain abscess, examination of the abscess fluid-
obtained by stereotactic aspiration or surgical excision of the abscess) for gram stain and culture is essential
.in HIV-positive Pts., 90% of brain lesions will be either toxoplasmosis or lymphoma
.viral upper respiratory infection can cause edema of the eustachian tube, which often leads to middle ear infection
.M.C organisms are streptococcus pneumoniae, H.influenzae and moraxella catarrhalis
+This is roughly the same breakdown of organism type and frequency that occurs in bronchitis and sinusitis
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-Diagnosis :
.physical examination of the ear is the chief means of establishing the diagnosis
.radiologic tests are not useful
.a specific bacteriological diagnosis can be obtained with tympanocentesis for culture, but this is rarely performed
-Treatment :
.oral therapy with amoxicillin is still the best initial therapy
.amoxicillin-clavulanate is used if there has been recent amoxicillin use or if the Pt. does not respond to amoxicillin
*Sinusitis
-An infection of the sinuses. The M.C site is the maxillary sinus, followed by ethmoid, frontal and sphenoid sinuses
-Signs & Symptoms :
.facial pain
.headache (is common and is worse when the Pt leans forward)
.postnasal drainage
.purulent nasal drainage
.fever
.tooth pain
-Causes :
.viruses are responsible for a large number of cases
.bacterial organisms cause disease with the same frequency as in otitis media described above
-Diagnosis :
.do not always need radiologic confirmation prior to treatment
.sinus x-ray are of little value, and routine imagine as a rule is not recommended
.CT scan of the sinuses is the test of choice
.sinus puncture is necessary to confirm a specific bacteriologic etiology
-Treatment :
.decongestants, such as (oral pseudoephedrine or oxymetazoline sprays) (for mild or acute uncomplicated sinusitis)
.antibiotics (for severe pain with discolored nasal discharge)
+Most cases of viral rhinosinusitis resolve in 7-10 days with asymptomatic management (antihistamines, NSAIDs and
decongestants)
*Pharyngitis
-The majority of pharyngeal infections are from viruses, the most important cause is from group A beta-hemolytic
streptococcus (S.pyogenes)
-Signs & Symptoms :
.sore throat with cervical adenopathy
.inflammation of the pharynx with an exudative covering is highly suggestive of S.pyogenes (Most viruses do not give an
exudate, although the Epstein-Barr virus can / Mild S.pyogenes infections may not give an exudate)
.hoarseness and cough are not suggestive of pharyngitis
-Diagnosis :
.rapid streptococcal antigen test are 60-100% sensitive but are >95% SPECIFIC
-Treatment :
.penicillin
*Influenza
-A systemic viral illness from influenza A or B, usually occurring in an epidemic pattern and transmitted by droplet nuclei
+Influenza can lead to damage to the respiratory epithelium, leading to sinusitis, otitis media, bronchitis and pneumonia
-Signs & Symptoms :
.fever
.myalgias
.headache and fatigue
.upper respiratory symptoms tend to predominate
.runny nose (coryza)
.nonproductive cough
.sore throat
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.conjunctival injection
-Diagnosis :
.rapid antigen swabs or washings of nasopharyngeal secretions
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.viral culture is the most accurate test but is usually not available rapidly enough to make it useful in acute Pt management
-Treatment :
.symptomatic therapy with acetaminophen and antitussives is useful
.specific anti-viral medications for both influenza A and B are the (neuraminidase inhibitors oseltamivir and zanamivir) – they
should be used within 48hrs of the onset of symptoms to limit the duration of symptoms
+Influenza vaccine is contraindicated in those who are highly allergic to eggs and which would result in anaphylaxis
**Gastrointestinal Infections
*Infectious Diarrhea/Food Poisoning
-Diarrhea (is the condition of having three or more loose or liquid bowel movements per day)
+Diarrhea is most commonly due to viral gastroenteritis with rotavirus, which accounts for 40% of cases in children under five
-Most infectious is caused by contaminated food and water, so the overlap between food poisoning and infectious diarrhea is
considerable
+There are several types of food poisoning, such as with Bacillus cereus or Staphylococcus aureus, that present predominantly
with vomiting, so the tow are not entirely synonymous
+Complications Of Diarrhea :
.dehydration
.acidosis (normal anion gap)
.electrolyte disturbances (decreased K+, increased Na+, decreased Cl-)
.hemoconcentration (increases hematocrit)
+Types Of Diarrhea :
1.Secretory (M.C.C of this type of diarrhea is a cholera toxin – that stimulates the secretion of anions, especially chloride ions)
2.Osmotic (can be the result of maldigestion – pancreatic disease or celiac disease) (it can be caused by osmotic laxatives)
(lactose intolerance – lactase deficiency)
3.Exudative (occurs with the presence of blood and pus in the stool)
4.Motility-related (is caused by the rapid movement of food through the intestinal – hypermotility) (diabetic neuropathy,
hyperthyroidism, increased peristalsis)
-Signs & Symptoms :
.the single most important feature of any person presenting with possible food poisoning is the presence or absence of blood in
the stool
.blood is most commonly associated with invasive enteric pathogens, such as (Salmonella, Shigella, Yersinia, invasive E.coli and
Campylobacter)
.ingestion of ciguatera toxin causes symptoms within 2-6 hrs, which includes (paresthesias, numbness, nausea, vomiting and
abdominal cramps). In severe cases they can be neurologic (weakness, reversal of hot-cold sensations), and cardiovascular
(hypotension) can develop
.Bacillus cereus and Staphylococcus predominantly present with vomiting 1-6hrs of their ingestion because they contain a
preformed toxin. They can give diarrhea later
.Giardia, Cryptosporidium, Cyclospora and most other protozoans do not give bloody diarrhea (the major protozoan associated
with blood in the stool is Entamoeba histolytica)
.Viruses can give voluminous watery diarrhea but do not result in bloody diarrhea
-Causes :
.Campylobacter (M.C)
.Salmonella (associated with contaminated poultry and eggs)
.E.coli (M.C.C of travelers` diarrhea)
.E.coli 0157:H7 (associated with eating under-cooked hamburger meat and with hemolytic uremic syndrome HUS)
.Shigella (associated with hemolytic uremic syndrome HUS)
.Bacillus cereus (associated with fried rice)
.Giardia lamblia and Cryptosporidiosis (are acquired from contaminated water sources that have not been appropriately
filtered, such as that ingested from fresh water on a camping trip)
.Cryptosporidiosis (associated with HIV, particularly when there is profound immunosuppression and the CD4 count has
dropped below 50 cells)
.V.parahaemolyticus (associated with contaminated shellfish, such as clams, oysters and mussels)
.V.vulnificus (from ingestion of raw shellfish) causes severe disease in those who have underlying liver disease. Is also
154
(associated with iron overload and the development of bullous skin lesions)
.viral infectious such as with rotavirus or Norwalk agents are most commonly (associated with outbreaks in children
.C.difficile (associated with previous antibiotic use)
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*Gastroenteritis
-Viruses (rotavirus) and the bacteria (E.coli, Campylobacter) are the primary causes of gastroenteritis
+Rotavirus is the M.C.C of gastroenteritis in children's (VIRAL)
+Campylobacter jejuni is the M.C.C of gastroenteritis in adults (BACTERIAL)
+E.coli, Salmonella, Shigella, Campylobacter are the M.C types can cause gastroenteritis in children's (BACTERIAL)
+Toxigenic Clostridium Difficile is an important cause of diarrhea (associated with antibiotic use) (treated by vancomycin)
+Enterotoxigenic Escherichia coli (is most commonly isolated pathogen – Traveler's diarrhea) (Traveler's diarrhea is NOT bloody
diarrhea)
+Giardia lamblia, Entamoeba histolytica (treated by metronidazole) and (Cryptosporidium-M.C.C for diarrhea in AIDS Pts.)
(PARASITIC)
+Bloody Diarrhea (E.coli, Shigella, Salmonella, Campylobacter, ameba)
+Clostridium botulinum (associated with canned food) (appear 18-24hrs / after 24hrs)
+Clostridium perfringens (appear 18-24hrs / after 24hrs))
+Staphylococcus aureus (M.C.C for food poisoning) (appear 1-6hrs / after 24hrs)
+Bacillus cereus (associated with rice) (appear 1-6hrs / after 24hrs)
+Treatment (Antimotility agents - are drugs used to alleviate the symptoms of diarrhea) (loperamide) (loperamide is not
recommended in children or bloody diarrhea) / (Antiemetic - is a drug that is effective against vomiting and nausea)
(Ondansetron-zofran) (Metoclopramide-clopram, plasil)
+Food poisoning :
.Salmonella food poisoning is common
.Incubation period of salmonella food poisoning is 12-48 hours
.Incubation period of staphylococcal food poisoning is 1-8 hours
.Amanita poisoning is a type of mushroom poisoning
+Cause Food Poisoning By Causing Gastrointestinal Tract Infection :
.Salmonella
.Staphylococcus
.Vibrio parahaemolyticus
.Fungus
+Cause Food Poisoning By Producing Toxin :
.Staphylococcus
.Clostridium perfringens
.Clostridium botulinum
.Bacillus cereus
+Feature Of Staphylococcal Food Poisoning :
.Abdominal cramps
.Hypotension
.Vomiting
.Diarrhea
+Staphylococcal food Poisoning :
.Contaminated meats and confectionery constitute the most outbreak
.Vomiting and severe abdominal cramps are prominent symptoms
.The acute symptoms usually subside within 12 hours
.Majority of patients require no specific treatment
.Short incubation period
.It is a common source-type of epidemic
155
+The characteristic incubation period for staphylococcus aureus food poisoning is 1-6hrs
+The incubation period of a food poisoning by chemical poisons is usually less than 1 hr
+Coliform organisms are used for routine testing of water
+Causes Of Invasive Diarrhea :
.Salmonella
.Campylobacter
.Shigella
.Amebiasis
++Common Drugs
+Vancomycin is the best treatment for pseudomembranous colitis (associated with antibiotics use)
+Erythromycin is bacteriostatic antibiotic
+Cefepime is active against pseudomonas infection
+Infections with Giardia lamblia are best treated with Metronidazole
+Penicillin the drug of choice for a child with pneumococcal pneumonia
+Antiviral Drugs :
.Acyclovir
.Vidarabine
.Ganciclovir
.Interferon
.Zidovudine
+Hepatitis A (incubation period 2-6 weeks) (virus RNA) (onset - abrupt) (transmession - fecal/oral)
+Hepatitis B (4-26 weeks) (DNA) (insidious) (sexual > parenteral)
+Hepatitis C (2-20 weeks) (RNA) (insidious) (parenteral > sexual)
156
+Viral Hepatitis :
.Hepatitis B is transmitted by feco-oral route
.Vaccination is available for hepatitis C
.Hepatitis B is a DNA virus
.Interferon treatment is required for hepatitis E
.Hepatitis B are not RNA viruses
.Hepatitis B vaccine is given in 2 doses
.Vaccine is protective for maximum 10yrs after administration
.Vaccine offers also partial protection against hepatitis C infection
.Vaccine should not be used in children younger than 10yrs of age
.The incubation period of infectious hepatitis is over 15 days
.Hepatitis A is the commonest
.All viruses are RNA except hepatitis B is DNA
.Hepatitis A and E don't produce chronic illness
.Hepatitis C is responsible for most chronic cases
.The greatest risk for infection transmitted by blood transfusion is present in one of the Hepatitis C
+Hepatitis A :
.Infectious before the appearance of jaundice
.Transmitted by feco-oral route
.Cause marked elevation on the liver enzymes
.The disease gives long life immunity
.Infectivity is high before the appearance of jaundice
.The vaccine is available after the age of one year
.In small children most cases are anicteric
.May present an anicteric in some cases less than 5yrs of age
.No specific treatment needed in most cases (prognosis is usually good)
+Hepatitis B :
.May be transmitted sexually
.Can cause chronic active hepatitis
.Hepatoma is recognized complication
.Vaccination is available
.Caused by DNA virus
.Produces chronic hepatitis in 5-10% of cases
.Infection has longer incubation period than hepatitis A
.Infection can be prevented by the use of vaccine
.May be transmitted sexually
.Hepatoma is recognized complication
.Vaccination is available
+Causes Of Chronic Hepatitis :
.Hepatitis B
.Hepatitis C
.Methyldopa
.Alpha-1-antitrypsin deficiency
+In Hepatocellular Carcinoma :
.It may lead to cirrhosis
.It leads to increased alfa feto protein
.It may cause fever
.It can be associated with polycythemia
*Syphilis
A systemic contagious disease caused by a spirochete; characterized by periods of active manifestations and by periods of
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symptomless latency
-Signs & Symptoms :
1.Congenital
.early (symptomatic seen in infants up to two years)
.late (symptomatic, hutchinson teeth, scars of interstitial keratitis, bony abnormalities - saber shins)
2.Acquired
.early infectious syphilis (primary stage – chancre that appears within the 3 rd week and disappears within 10-90 days.
Lymphadenopathy is painless, rubbery, discrete and nontender to palpation. Primary chancres are usually found on the penis,
anus, rectum in men, and vulva, cervix, and perineum in women (may be found in other places such as lips, tongue, ect.)
(secondary stage – cutaneous rashes appear 6-12 weeks after infection, usually found symmetrically and more marked on the
flexor and volar surfaces of the body-pinkesh or pale red in white persons, pigmented spots, copper-colored macules in blacks /
lymphadenopathy, papules and alopecia can be seen)
.latent stage (may persist for life, and one-third of Pts. develop late or tertiary syphilis)
.late or tertiary syphilis (most commonly neurologic)
-Causes :
.Treponema pallidum
-Diagnosis :
.screening tests are the VDRL and RPR
.specific tests are the FTA-ABS, MHA-TP and dark field exam of chancre
-Treatment :
.penicillin (drug of choice for all stages of syphilis)
+A reaction called Jarisch-Herxheimer (general malaise, fever, headache, sweating rigors, and temporary exacerbations of the
syphilitic lesions 6-12hrs after initial treatment)
*Chancroid
-An acute, localized, contagious disease characterized by painful genital ulcers and suppuration of the inguinal lymph nodes
-Signs & Symptoms :
.small, soft, painful pimples that become shallow ulcers with ragged edges
.inguinal lymph nodes become very tender and enlarged
-Causes :
.Haemophilus ducreyi (Gram-negative bacilli)
-Diagnosis :
.made on clinical findings usually Gram stain initially with culture to confirm
.PCR testing is useful
-Treatment :
.azithromycin (single dose)
.ceftriaxone intramuscularly (single dose)
.erythromycin for 7 days or cipro for 3 days are alternative
*Genital Herpes
-Herpes virus, type 2, although type 1 can be seen in genital herpes
-Clinical Presentaion :
.vesicles develop on the skin or mucous membranes; they become eroded and painful and present with circular ulcer with a red
areola
.itching and soreness usually precede them
.the ulcer are scarring; there can be inguinal lymphadenopathy
.lesions are commonly seen in the penis in males and on the labia, clitoris, perineum, vagina and cervix in females
-Diagnosis :
.tzanck test and culture
-Treatment :
.acyclovir, famciclovir or valacyclovir
*Genital Warts
158
.more common in women, in childhood, during pregnancy or after urethral catheterization or instrumentation
.E.coli is the most common pathogen, others include (klebsiella, proteus and enterococcus)
+Pts. who are immunosuppressed and subjected to indwelling catheters are more prone to candida
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**Skin Infections
*Impetigo
-A superficial, pustular skin infection seen mainly in children (ecthyma is an ulcerative form of impetigo), with oozing, crusting
and draining of the lesions
-Signs & Symptoms :
.more common on arms, legs and face
.may follow trauma to skin
.begins as maculopapular and rapidly progresses too vesicular pustular lesions or bullae
.the crusts are described as having a golden or yellow appearance and if untreated can progress to lymphangitis, furunculosis or
cellulitis and acute glomerulonephritis (due to gas)
-Causes :
.group A beta-hemolytic Streptococcus
.S.aureus (bullous impetigo)
-Treatment :
.oral first-generation cephalosporin or semisynthetic penicillin, oxacillin, cloxacillin, dicloxacillin (for severe or widespread cases)
.topical mupirocin or bacitracin for mild cases
.penicillin-allergic Pts can be treated with macrolides such as clarithromycin or azithromycin
*Candidiasis
*Scabies
.the earliest tests to detect osteomyelitis are the technetium bone scan and the MRI (but the MRI can allow better
differentiation between the overlying soft-tissue infection and bone)
.x-ray (usually the initial test because it is more easily)
.erythrocyte sedimentation rate ESR (nonspecific – it is useful to follow during treatment)
.CT scan, indium and gallium (all three can be normal in osteomyelitis, but none are as specific or sensitive)
-Treatment :
.acute hematogenous osteomyelitis in children can usually be treated with antibiotics alone
.in adults (combination of surgical – wound drainage and debridement, removal of infected hardware) and antibiotic therapy
(treatment for 6-12 weeks)
.chronic osteomyelitis must be treated for as long as 12 weeks of antibiotics therapy, and in some cases, even longer periods of
antibiotics may be required
*Septic Arthritis
-Infection of a joint due to virtually any agent. The M.C etiology is bacteria (Neisseria gonorrhoeae, Staphylococci or
Streptococci) but (Rickettsia, Viruses, Spirochetes, ect. May also cause it). Generally, bacterial arthritis is divided into
Gonococcal and Non-Gonococcal types
-Pathogenesis :
.sexual activity is the only significant risk factor for gonococcal septic arthritis. Nongonococcal bacterial arthritis is usually
spread by the hematogenous route. Additional routes may include bites (animal or human), direct inoculation of bacteria into
the joint through surgery or trauma, or spread infection from surrounding structures such as bone
.even though both normal or damaged joints can get infected, any previous damage to a joint, such asa from rheumatoid
arthritis or osteoarthritis, previous surgery, prosthesis placement, gout, sickle cell disease, or the presence of certain risk factors
such as intravenous drug abuse, DM or HIV infection can predispose a joint to infection (any cause of bacteremia can seed the
joint because the synovium does not have a basement membrane)
-Presentation :
.Non-Gonococcal (monoarticular in >85%, with a swollen, tender, erythematous joint with a decreased range of motion. Knee is
the M.C. Skin manifestations are rare)
.Gonococcal (polyarticular in 50%; a tenosynovitis is much more common. Effusions are less common. Migratory polyarthralgia
are common. Skin manifestation with petechiae or purpura are common)
-Diagnosis :
.Non-Gonococcal (culture of joint aspirate fluid is positive in 90-95% and gram stain is positive in 40-70%. The cell count of the
synovial fluid is high >500.000 and is predominantly PMNs with a low glucose. Blood culture is positive in 50%)
.Gonococcal (much harder to culture. Only 50% aspirates have positive synovial fluid culture. Less than 10% of blood cultures
are positive. Other sites such as cervix, pharynx, rectum and urethra may also be positive. In the aggregate, culture of the other
sites has a greater yield than culturing the joint itself)
-Treatment :
.Non-Gonococcal (nafcillin or oxacillin vs vancomycin if MRSA is suspected)
.Gonococcal (ceftriaxone is the drug of choice)
**Carditis
*Infective Endocarditis
-Colonization of heart valves with microbial organisms causing friable infected vegetations and valve injury / Bacterial
endocarditis produces large vegetations and may affect any value in the heart, although left-sided lesions of the aortic and
mitral valves are common
-Signs & Symptoms :
161
.chills, sweats, fever, dyspnea, cough, stroke, skin lesions, nausea and vomiting, chest pain, malaise
.heart murmur or changing murmur
.splenomegaly
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.septic complications
.mycotic aneurysm
.glomerulonephritis
.digital clubbing
.retinal lesions
.petechiae (streptococcus, staphylococcus)
.splinter hemorrhages (streptococcus, staphylococcus)
.osler`s nodes (streptococcus)
.janeway lesions (staphylococcus)
.roth`s spots (streptococcus)
-Cuases :
.dental procedures that cause bleeding
.oral and upper respiratory tract surgery
.certain gastrointestinal procedures
.genitourinary surgery
.prosthetic heart valves
.virtually any valvular heart disease
.alimentation catheters in the right heart
.intravenous drug use
+Acute Infective Endocarditis
.caused by bacteremia
.S.aureus is the M.C.C of acute endocarditis
.produces large, bulky vegetations (2mm to 2cm) on the atrial side
.IV drug use the major risk factor
.rapid onset with fever and sometimes sepsis
.splenomegaly
.associated with invasion of myocardium (abscess cavities) and rapid valve destruction
+Subacute Infective Endocarditis
.4-5% have negative blood cultures
.risk factors (ventricular septal defect with shount/stenosis of any valve/prosthetic valves/indwelling catheters/bicuspid aortic
valve/mitral valve prolapse/marfan syndrome)
-Complications Of Infective Endocarditis :
.congestive heart failure (M.C.C of death)
.septic embolization (related to infarctions and metastatic infections); brain (mycotic aneurysm); spleen (greater with
subacute); kidneys; coronary arteries
.glomerulonephritis with nephrotic syndrome or renal failure (immune complex)
-Diagnosis :
.the major criteria for the diagnosis of endocarditis are a combination of positive blood cultures and an abnormal echo
.the minor criteria (fever, intravenous drug use, vascular phenomena, immunologic phenomena, microbiological evidence)
*Pericarditis
-Infection of inflammation of the pericardium
-Signs & Symptoms :
.sharp, pleuritic, retro-sternal (under the sternum) or Lt. precordial (Lt. chest pain)
.Pain is worse in the supine position or upon inspiration
.friction rub (auscultated on the cardiovascular examination usually on the lower Lt. sternal border)
.low-grade fever may also be present
.with tamponade (pulsus paradoxus)
-Causes :
+Pericarditis may be caused by (Viral, bacterial or fungal infection)
.M.C viral (Coxsackie-virus)
.M.C bacterail (Pneumococcus or tuberculous pericarditis)
+Others :
.idiopathic are probably viral
.immunologic conditions (SLE, RF) (SLE more in women)
162
-Diagnosis :
.ECG (diffuse ST segment elevation. The ST elevation progresses to T-wave inversion)
+Echo (may be normal in viral)
-Treatment :
.for viral or idiopathic pericarditis (inti-inflammatory medication like indomethacin, ibuprofen or naprosyn) (NSAIDs-aspirin)
.adequacy of response to antiretroviral medications (the best test to monitor response to therapy os the HIV-RNA viral load)
-Viral Load Monitoring :
.viral load can be compared to glucose level for Pts. with diabetes
.monitoring of viral load is the best method to monitor adequate response to therapy when the Pts. is on antiretroviral
medications and the goal is undetectable viremia
.a high viral load generally indicates that the level of CD4 cells is going to drop more rapidly
-Viral Sensitivity / Resistance Monitoring :
.is done to determine which antiviral medications will be effective in an individual Pt.
.sensitivity testing should always be done if a Pt is failing a combination of medications and a change in therapy is necessary
.it should also be done in any pregnant woman who has not been fully suppressed on the initial combination of medications
-Pregnant Pts. :
.pregnant women with serious disease (low CD4 or high viral load) should be treated fully for their HIV infection. That is, they
should get triple antiretroviral therapy as you would in a non pregnant person)
.C/S is only used routinely in those whose CD4 count and viral load are not controlled with medications (when viral load is
>1000 copies/mL of HIV-RNA at the time of delivery)
.zidovudine (AZT) treatment is indicated in all pregnant women. This should be used in combination with tow other
antiretroviral medications
-Breast Feeding :
.breast feeding is associated with transmission of virus to the infant. If a pregnant woman is already on antiretrivirals, she
should continue
.the majority of women can delivery with a normal vaginal delivery
+NOTES :
.It is associated with a very high viral load
.It occurs in at least 70% of HIV infection
.Maculopapular rash can occur in the upper trunk
.It is diagnosed by viral PCR
.It is transmitted by sexual contact
.It can be transmitted by blood transfusion
.The incubation period varying from one year to ten years
.Kaposi's sarcoma can occur
.Can be transmitted from mother to fetus
.Is caused by retrovirus
.Causes dementia
.Pneumocystis carinii pneumonia is a recognized complication
.May be transmitted through kidney transplantation
.Carriers are infectious
.Affects mainly the helper T-cells (T4)
.Affect the central nervous system
.Most common risk factors are MSM and heterosexual intercourse
.In women, the most common mode is heterosexual transmission
.There is often a 10-yrs lag between contracting HIV infection and developing the first symptoms. This is because CD4 cells drop
at a rate of 50-100/mL/yr without therapy
**Tetanus
-A severe infectious complication of wounds caused by the toxin of Clostridium tetani (neurotoxin); takes 1-7 days to develop;
spore forming, Gram-positive rod
-Signs & Symptoms :
.tonic spasm of voluntary muscles
.respiratory arrest
.difficulty in swallowing (dysphagia)
.restlessness
.irritability
.stiff neck, arms and legs
.headache
.lockjaw
165
.flexion of the arms and extension of the lower extremities, and high mortality rate
-Diagnosis :
.clinical
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-Treatment (prophylaxis)
.tetanus toxoid – boosters every 10 yrs)
.immediate surgical care, debride wound
.antitoxin, tetanus immunoglobulin
.penicillin 10-14 days
+NOTES :
.Trismus is characteristic
.The longer incubation period is better in the prognosis
.CSF is usually normal
.If the patient survives, recovery is complete
.It is the result of wound infection by gram-positive anaerobic bacilli of clostridia group
.These organisms live normally and actively in soil
.The usual cause of death in established tetanus is respiratory failure
.There are exotic noninvasive organism
.This disease is best prevented by active immunization and proper wound management
.The usual cause of death is established tetanus is respiratory failure
.Mild cases of tetanus can be treated with tetanus immunoglobulin IV or IM
.The cause of death in established tetanus is respiratory failure
.To prevent tetanus neonatorum women should be actively immunized by puberty
.Recommended for universal use regardless of age
.Important for workers in contact with soil, sewage or domestic animals
.For severe wounds, give a booster if more than 5Yrs have elapsed since the last dose
+Diseases May Be Water-Borne :
.Typhoid fever
.Bacillary dysentery
.Cholera
.Infectious hepatitis (hepatitis A)
.Tetanus (except)
HEMATOLOGY
**ANEMIA
-A hematocrit (Hct) less than 41% in men / less than 36% in women
-A hemoglobin less than 13.5gm/dL in men / less than 12 mg/dL in women
+Microcytic (MCV <80) :
.iron deficiency
.thalassemia
.sideroblastosis
.lead poisoning
.anemia of chronic disease (can be either microcytic or normocytic)
+Mactocytic (MCV >100) :
.vit B12
.folic acid deficiency (but can also result from the toxic effects of alcohol)
.liver disease
.chemotherapeutic agents (methotrexate or zidovudine AZT or phenytoin)
.hypothyroidism
+Normocytic (normal MCV) :
.hemolysis
.aplastic anemia
+Hemolytic (Hymolysis) :
.Hereditary spherocytosis
.Hereditary elliptocytosis
.Sickle cell anemia
.Glucose-6-phosphate deficiency
+Hematocrit (Hct) (male 42%-54% / female 38%-46% / 1 year old age 20%-41%)
+Anemia is considered when RBCs count (< 4.5 million in males / < 3.9 million in females)
+Or Hemoglobin ( Hb ) content (< 13.5 gm % in males / < 11.5 gm % in females)
-Signs & Symptoms :
.fatigue
.tiredness
.poor exercise tolerance
.dyspnea on exertion and lightheadedness
.confusion and altered mental status may develop as oxygen delivery to the brain decreases
.death from anemia is most often from decreased oxygen delivery to the heart, resulting in the development of myocardial
ischemia
.a healthy young Pt. May have no symptoms at all with a hematocrit of 27-29%, whereas an older Pt. With heart disease may
develop dyspnea or anginal symptoms with the same hematocrit
-Diagnosis :
.once a diagnosis of anemia is determined based on a low hematocrit or hemoglobin
.MCV
.iron
.reticulocyte count
.peripheral smear
.red cell distribution of width (RDW)
.coombs test
.Vit B12
.folate levels
.bone marrow biopsy
167
-Treatment :
.a healthy young Pt. Can have transfusion withheld until the hematocrit is in the low 20%
.an older Pt. With coronary artery disease will need to be maintained above a hematocrit of 30%
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**MICROCYTIC ANEMIA
*Iron Deficiency Anemia
-Is defined as a decrease in the amount of red blood cells (RBCs) or hemoglobin in the blood due to not enough iron
+Is the commonest type of anemia in Jordan
+The average daily iron intake is 10-20 mg
+Iron absorbed in duodenum
+Alcohol increases iron absorption (tea drink are NOT)
+Ferrous iron absorbed better than ferric
-Signs & Symptoms (non-specific symptoms) :
.symptoms of fatigue and poor exercise tolerance may develop
.tachycardia
.palpitation
.dyspnea on exertion
.pallor develop
.older Pts. And those with coronary artery disease may become dyspneic at higher levels of hematocrit
.more severe anemia results in lightheadedness, confusion, syncope, and chest pain
.a systolic ejection murmur ‘flow murmur’ may develop in any Pt with moderately severe anemia
-Causes :
.is almost always caused by increased level of blood loss from the body
.the most common type of blood loss is gastrointestinal or menstrual
.a man requires about 1mg per day and a women about 2-3 mg per day on average
.it is difficult for the body to increase the level of iron absorption (occult blood in the stool, a heavier menstrual flow, or an
increased demand such as during pregnancy), the body is poorly equipped to increase its level of absorption to exceed 3-4 mg
per day
.other etiologies are increased urinary loss of blood, malabsorption, hemolysis and poor oral intake
-Symptoms specific to iron deficiency are very rare :
.brittle nails
.spoon shaped nails
.glossitis
.pica
+(iron def. Anemia as a specific diagnosis is determined by laboratory findings, not symptoms)
.High iron binding capacity
.Low serum ferritin
.Missed menstrual cycle
.Angular cheilitis (inflammatory lesions at the mouth's corners)
.Koilonychia (spoon-shaped nails) or nails that are weak or brittle
.Pruritus (itchiness)
.Insomnia
.Restless legs syndrome
-Treatment :
.oral therapy with ferrous sulfate tablets is the most common method of therapy
.parenteral iron is used in Pts with malabsorption, and in those who cannot tolerate oral therapy
.blood transfusion is the most effective method of delivering iron (but is not a standard method of correcting iron deficiency)
-Diagnosis :
.the serum ferritin level (is normal or elevated)
.the serum iron level and total iron binding capacity (TIBC) (are both low)
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*Sideroblastic Anemia
-A microcytic anemia caused by a disorder in the synthesis of hemoglobin characterized by trapped iron in the mitochondria of
nucleated red blood cells
+Is a form of anemia in which the bone marrow produces ringed sideroblasts rather than healthy red blood cells (erythrocytes)
-Signs & Symptoms :
.the symptoms are related to the severity of the anemia as described above
.there is no specific presenting findings that will be sufficiency suggestive of sideroblastic anemia to allow a diagnosis without
significant laboratory evaluation
-Causes :
.the hereditary is from either a defect in aminolevulinic acid synthase or an abnormality in Vit B6 metabolism
.acquired forms are from drugs such as chloramphenicol, isoniazid or alcohol
.lead poisoning can cause sideroblastic anemia as well
.there is an association with myelodysplastic syndromes (MDS) and refractory anemia
.these can progress to acute myelogenous leukemia in a small percentage of Pts.
.alcohol use (M.C.C of sideroblastic anemia)
.genetic syndromes
-Diagnosis :
.the ferritin level is elevated
.the serum iron level is high
.TIBC total is low
.the most specific test is a Prussian Blue stain of red blood cells in the marrow (Marrow reticuloendothelial iron is strikingly
increased)
-Treatment :
.pyridoxine
.treat the lead poisoning
.some Pts. with the hereditary form will respond to pyridoxine therapy 2-4mg per day
*Thalassemia
-Is a form of inherited autosomal recessive blood disorder characterized by abnormal formation of hemoglobin
+The abnormal hemoglobin formed results in improper oxygen transport and destruction of red blood cells / Thalassemia are
not acquired anemia
+The hereditary underproduction of either the alpha or beta globin chains of the hemoglobin molecule resulting in a
hypochromic, microcytic anemia)
-Signs & Symptoms :
.in alpha thalassemia one gene deleted yields a normal Pt. The CBC is normal, the hemoglobin level is normal, and the MCV is
normal
.tow genes deleted have a mild anemia with hematocrit ranging from 30-40% with a strikingly low MCV
.three genes deleted have more profound anemia with hematocrit between 22-32% as well as the very low MCV
.four genes deleted Pts. die in utero secondary to gamma chain tetrads called hemoglobin barts
.Pts. with beta thalassemia major are homozygous for mutations of both genes coding for the beta hemoglobin gene, these Pts.
with beta thalassemia major, also known as cooley anemia, become severely symptomatic starting at 6 months of age (Pt.
becomes symptomatic in the second 6 months)
.they are severely symptomatic with growth failure, hepatosplenomegaly, jaundice and bony deformities secondary to
extramedullary hematopoiesis, cirrhosis, CHF
.beta thalassemia – ‘hair on end’ appearance (skull x-ray)
.hemolytic anemia resulting from imbalance of alpha and beta globin chains
-Causes :
.there are four genes coding for the alpha chain of hemoglobin. There can be deletions of one, tow, three, or all four genes
(alpha is more common in asian populations / chromosome 16)
.beta thalassemia can be mutated in either one or tow genes (is more common in mediterranean populations / chromosome
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11)
-Diagnosis :
.beta thalassemia major has the severe symptoms, large spleen, and bone abnormalities described above
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.both forms of thalassemia are diagnosed by having a microcytic anemia with normal iron studies
.beta thalassemia, there is an increased level of hemoglobin F and hemoglobin A2 (hemoglobin is a low as 3-4g/dL)
.those with alpha thalassemia will have normal amounts of hemoglobin F and A2
.tetrads of beta chains are called hemoglobin H (hemoglobin H is present in alpha thalassemia with three of four genes deleted)
.RDW is normal in all forms because all of the cells are of the same size
-Treatment :
.beta thalassemia major Pts. require blood transfusions once or twice a month
.the chronic transfusions lead to iron overload, which requires treatment with deferasirox
.a small number of Pts can be treated with a bone marrow transplantation
**MACROCYTIC ANEMIA
*Vitamin B12 (cyanocobalamine) Deficiency
-Decreased absorption or intake of Vit B12 resulting in hematologic and/or neurologic abnormalities
-Signs & Symptoms :
.you cannot specifically determine that a Pt. has B12 deficiency only from the symptoms of anemia. Neurologic manifestations
may involve almost any level of the neurologic system
.Pts. may have peripheral neuropathy, position sense abnormality, viberatory, psychiatric, autonomic, motor, cranial nerve,
bowel, bladder and sexual dysfunction
.glossitis, diarrhea and abdominal pain may occur
.inadequate dietary intake of vitamin B12
.atrophic gastritis (in which case, the resulting megaloblastic anemia takes the name of "pernicious anemia"), or may result
from wide surgical resection of stomach
.resection of the terminal ileum (the principal site of vitamin B12 absorption)
.surgical removal of the small bowel
.long-term use of ranitidine hydrochloride
.Celiac disease
-Causes :
.the M.C.C of B12 deficiency is pernicious anemia
.the incidence of pernicious anemia increases with age. Gastrectomy and atrophic gastritis can also decrease intrinsic factor
production
.various forms of malabsorption such as sprue, regional enteritis, and blind loop syndrome can block absorption of Vit B12
.pancreatic insufficiency can result in the inability to absorb the Vitamin
.rarely, tapeworm infection with Diphyllobothrium latum can decrease absorption
.decreased intake is unusual and requires several years to produce disease
-Diagnosis :
.increased MCV, WBCs have hypersegmented neutrophils with a mean lobe count greater than four, RBCs are characterized by
macro-ovalocytes
.macrocytosis can occur with hemolysis liver disease and myelodysplasia
.reticulocyte count is reduced, although the bone marrow is hypercellular, pancytopenia may occur
.elevated LDH, bilirubin and iron level may occur but are nonspecific
.the most specific test is simply a low B12 level
.the Schilling test is occasionally used to determine the etiology of Vit B12 deficiency
.an elevated methylmalonic acid level occurs with B12 deficiency and is useful if the B12 level is equivocal
-Treatment :
.folic acid replacement can correct the hematologic abnormalities of B12 deficiency, but not the neurologic abnormalities
+Features Of Pernicious Anemia :
.Usually over 30 years, with blue eyes (elderly)
.Subacute combined degeneration of the cord can occur
.Optic atrophy can occur
.Weight loss is a common feature
.Subacute combined degeneration can occur
.Gastric atrophy with achlorhydria
+Significant in blood film is (hypersegmented neutrophils)
+The major difference between Vit12 and folate deficiency is (neuropathy-foot paresthesia)
170
intestine
-Signs & Symptoms :
.women with folate deficiency who become pregnant are more likely to give birth to low birth weight premature infants, and
infants with neural tube defects. neural tube defects
.symptoms dependent on the severity of the anemia
-Causes :
.is almost due to some form of decreased dietary intake
.increased requirements from pregnancy, skin loss in disease like eczema, or increased loss from dialysis may occur and certain
anticonvulsants, such as phenytoin
.alcoholics have decreased folate intake
.crohn's disease, coeliac disease
.tetrahydrofolic acid
-Diagnosis :
.the hematologic presentation of folic acid deficiency is identical to B12 deficiency
.the diagnosis is based on a low RBCs, folic-acid level
-Treatment :
.replace folic acid, almost always orally
+About Megaloblastic Anemia :
.megaloblastic anemia secondary to folate deficiency
.serum folic acid and vitamin B12 are not normal
.manifestation may appear in the first year of life
.white blood cells and platelets are normal
.occasionally treatment is required for life
.in Jordan goat's milk may be a factor in its etiology
**HEMOLYTIC ANEMIA
-Is a form of anemia due to hemolysis, the abnormal breakdown of red blood cells (RBCs), either in the blood vessels
(intravascular hemolysis) or elsewhere in the human body (extravascular)
-Signs & Symptoms :
.fatigue and weakness occur with mild disease
.dyspnea and later confusion occur with more severe disease
.shortness of breath
.jaundice and dark urine
.gallstones
.pulmonary hypertension
.fever, chills, chest pain, tachycardia and backache may occur if the intravascular hemolysis is particularly rapid
.the major difference between hemolytic anemia and the micro-and macrocytic anemias is that hemolysis is more often the
etiology when the onset is sudden
-Causes :
.hemolytic anemia may either be chronic as in sickle cell disease, paroxysmal nocturnal hemoglobinuria, and hereditary
spherocytosis or acute such as in drug-induced hemolysis, autoimmune hemolysis, or G6PD deficiency
-Diagnosis :
.Pts. with hemolytic anemias generally have a normal MCV (but may be elevated)
.the LDH and indirect bilirubin are elevated (bilirubin levels above 4 are unusual with hemolysis alone)
.the peripheral smear shows fragmented cells, and the haptoglobin may be low with intravascular hemolysis
.hemoglobin may be present in urine when intravascular hemolysis is sudden and severe because free hemoglobin spills into
the urine
-Treatment :
.transfusion is needed as in all forms of anemia when the hematocrit becomes low
+Hemolysis May Occur In (Hemolytic Anemias) :
.Hereditary spherocytosis
.Thalassemia
.Sickle cell anemia
.Glucose-6-phosphate deficiency
.Hereditary elliptocytosis
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drugs (the M.C drugs are the penicillins, cephalosporins, sulfa drugs, quinidine, alpha methyldopa, procainamide, rifampin and
thiazides
.cold agglutinin disease is an IgM antibody produced against the red cell in association with malignancies such as lymphoma or
waldenstrom macroglobulinemia and infections such as mycoplasma or mononucleosis
.UC can also lead to autoimmune hemolytic anemia
-Diagnosis :
.autoimmune hemolysis gives a normocytic anemia, reticulocytosis, increased LDH, absent or decreased haptoglobin, and
increased indirect bilirubin
*Herediatery Spherocytosis
-A chronic mild hemolysis (autosomal dominant disorder) with spherocytes,jaundice and splenomegaly from a defect in the red
cell membrane
-Hemolysis occurs in the spleen, there is often splenomegaly and jaundice
-Severe anemia occasionally occurs from folate deficiency or parvovirus B19 infection such as in sickle cell disease. Bilirubin
stones often occur, leading to cholecystitis, often at a young age
-Treatment :
.folate replacement
.with more severe anemia, removal of the spleen
*Aplastic Anemia
-Failure of all three cell lines produced in the bone marrow resulting in anemia, leukopenia and thrombocytopenia
(pancytopenia)
-Signs & Symptoms :
.Pts. most commonly present with bleeding from the thrombocytopenia, but may present with a combination of the findings
associated with deficiencies in all three cell lines
.fatigue from anemia and infections from neutropenia may also occur
.the clinical presentation may give a clue to presence of pancytopenia but is not sufficient to determine a true plastic anemia by
clinical manifestations alone
.the absence of a classical association such as benzene, radiation or chloramphenicol would most certainly not exclude a
diagnosis of a plastic anemia
.the most common single etiology is idiopathic
-Causes :
.there are many things that can cause bone marrow failure, the most common cause of true aplastic anemia is rarely precisely
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determined
.radiation, toxins such as benzene, drugs such as nonsteroidal anti-inflammatory agents, chloramphenicol, alcohol and
chemotherapeutic alkylating agents
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.infiltration of the bone marrow with infections such as TB or cancer such as lymphoma can cause pancytopenia (but this is not
truly aplastic anemia)
.infections such as hepatitis, HIV, CMV, EBV and parvovirus B19 in immunocompromised Pts.
-Diagnosis :
.pancytopenia on a CBC is the first test
.bone marrow biopsy confirms the diagnosis when alternative etiologies for a pancytopenia are not present (in other words, the
marrow is empty of almost all precursor cells as well as evidence of primary or metastatic cancer, infection or fibrosis)
.the marrow is hypoplastic and fat filled with no abnormal cells seen
-Treatment :
.bone marrow transplantation should be carried out whenever th Pt. is young and healthy enough to withstand the procedure
and there is a donor available
**ACUTE LEUKEMIA
-The rapid onset of bone marrow failure from the derangement of the pluiropotent stem cell resulting in the relentless
destruction of the normal production of the entire bone marrow. The blood cells lose the ability to mature and function
normally
-Signs & Symptoms :
.the M.C presentation results from the effects of the leukemic blast cells crowding out the normal marrow cells, resulting in
symptoms pf pancytopenia even if the total WBCs count is normal
.fatigue from anemia is the most common presenting complaint
.bleeding from thrombocytopenia occurs
.infections from the underproduction or abnormal function of white blood cells also occurs
.acute lymphocytic leukemia (ALL) is more common in children
.acute myelogenous leukemia (AML) is more common in adults
+ALL is more often associated with infiltration of other organs, but AML can do it as well
.enlargement of the liver, spleen and lymph nodes and bone pain are common at presentation
.disseminated intravascular coagulation DIC is associated with M3 promyelocytic leukemia
.CNS involvement resembling meningitis is present at the time of initial diagnosis in about 5% of Pts. (CNS involvement is most
characteristic of M4 and M5 monocytic leukemia)
.rarely, a syndrome of ‘leukostasis’ can occur when the white cell count is extremely elevated (resulting, in headache, dyspnea,
confusion and brain hemorrhage)
-Causes :
.most cases of acute leukemia arise with no apparent cause
.association with the development of acute leukemia, include (radiation exposure, benzene, chemotherapeutic agents such as
melphalan nad etoposide, as well as some retroviruses) (genetic disorders such as down syndrome and klinefelter can result in
an increased incidence of leukemia)
.myelodysplasia and sideroblastic anemia can also develop into acute leukemia
-Diagnosis :
.the CBC is the first clue to the diagnosis
.depression of all three cell lines is common at presentation
.the white cell count can be low, norma or elevated
.thrombocytopenia and anemia are usual
.many other disorders can present as pancytopenia similar to leukemia such as aplastic anemia, infections involving the
marrow, metastatic cancer involving the marrow, Vit B12 deficiency, SLE, hypersplenism and myelofibrosis
.a bone marrow biopsy showing greater than 20% blasts confirms the diagnosis of acute leukemia
.the presence of blasts tells you the Pt has acute leukemia (but blast analysis cannot be relied upon to always tell which type is
present)
.AML is characterized by the presence of Auer rods (Auer rods are most specific for M3), myeloperoxidase and esterase
.ALL is characterized by the presence of the common ALL antigen (CALLA) and terminal deoxynucleotidyl transferase TdT
.hyperuricemia and increased level of LDH
-Treatment :
.chemotherapy is used initially in all Pts. to induce a remission. Inducing a remission means a removal of over 99.9% of the
leukemic cells in the body
.the initial chemotherapy for AML is (cytosine arabinoside – AraC)
.the initial chemotherapy for ALL is (daunorubicin, vincristine and prednisone)
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.promyelocytic leukemia is managed with the addition of the Vit A derivative all-trans-retinoic acit ATRA)
.all Pts must also undergo prophylaxis of the CNS to prevent relapse there. The best agent for this is intrathecal methotrexate
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**CHRONIC LEUKEMIA
*Chronic Myelogenous Leukemia (CML)
-A chronic myeloproliferative disorder characterized by the massive overproduction of myeloid cells. These cells retain most of
their function until later in the course of the disease
-Is a cancer of the white blood cells. It is a form of leukemia characterized by the increased and unregulated growth of
predominantly myeloid cells in the bone marrow and the accumulation of these cells in the blood
+M > F, and appears more common in the elderly with a median age at diagnosis of 65 years
-Signs & Symptoms :
.elevated white blood cell count can be found on routine blood count
.the most common symptoms are fatigue, night sweats and low-grade fever
.abdominal pain from massive enlargement of the spleen is common
.bone pain from infiltration with white cells can occur
.enlarged lymph nodes are rare
.infections and bleeding are uncommon
.rarely, a leukostasis reaction can occur from extremely elevated amounts of white cells (20.000-500.000)
-Causes :
.philadelphia chromosome is characteristic of the disease, the cause of the production of this chromosome is unknown
.the philadelphia chromosome is a translocation between chromosomes 9 and 22, resulting in a gene producing an enzyme with
tyrosine kinase activity
.five percent of cases are philadelphia chromosome negative
-Diagnosis :
.elevated white blood cell count
.neutrophils with a left shift
.blasts are either absent or present in very small amounts <5%
.the leukocyte alkaline phosphatase score (LAP) is diminished
.basophilia is characteristic of CML and all myeloproliferative disorders such as polycythaemia vera
.level B12 elevated (this not be enough to establish the diagnosis)
.philadelphia chromosome is a far more specific test for CML and should be done in a Pt with a markedly elevated white cell
count and a low LAP score
.platelet count can also be markedly elevated
-Treatment :
.the best initial therapy for CML is imatinib (Gleevec)
**LYMPHOMA
*Hodgkin Disease
176
-A neoplastic transformation of lymphocytes particularly in the lymph node characterized by the presence of Reed-Sternberg
Cells on histology and to spread in an orderly
-Signs & Symptoms :
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.enlarged, painless, rubbery, non erythematous, non tender lymph nodes are the hallmark of the disease
.Pts may also develop what are labeled ‘B’ symptoms, which are drenching night sweats, 10% weight loss and fevers
.pruritus is common in the disease (it is not one of the ‘B’ symptoms)
.cervical, supraclavicular and axillary lymphadenopathy are the most common initial signs of disease
.extralymphatic involvement is more common with non-Hodgkin lymphoma
-Causes :
.there are no clear environmental or infectious etiologies for the disorder
.hodgkin disease has bimodal age distribution (one peak in the 20s and 60s)
-Staging is as follows (the staging is the same for both Hodgkin as well as non-Hodgkin lymphoma) :
.stage 1 (one lymphatic group or single extra lymphatic site
.stage 2 (two lymphatic groups or extra lymphatic sites on the same side of the diaphragm)
.stage 3 (involvement of lymphatic groups on both sides of the diaphragm or involvement of any extralymphatic organ
contiguous to the primary nodal site
.stage 4 (widespread disease with involvement of diffuse extralymphatic sites such as the bone marrow or liver)
-Diagnosis :
.an excisional lymph node biopsy is the essential first step in determining the diagnosis
.after the initial diagnosis (biopsy), the most important step is to determine the extent of the disease because the stage will
determine the nature of the therapy, that is radiation versus chemotherapy
.a CXR or chest CT scan, abdominal CT scan, or MRI are used to determine if the disease is localized to the supraclavicular area
.lymphangiography and laparotomy are no longer routinely used for staging (laparotomy is used to definitively exclude more
widespread disease)
.CT scanning is sensitive enough to detect any involved lymph nodes
.if all of these tests are unrevealing and localized radiotherapy is contemplated
.a bone marrow biopsy is also sometimes used to definitively determine if the disease is truly localized
-Treatment :
.localized disease such as stage 1 and 2 is managed predominantly with radiation
.all Pts with evidence of ‘B’ symptoms as well as stage 3 or 4 disease are managed with chemotherapy
.the most effective combination chemotherapeutic regimen for Hodgkin disease is ABVD
+Types :
.Nodular sclerosis (M.C subtype)
.Mixed cellularity
.Lymphocyte predominant (Lymphocyte-rich)
.Lymphocyte depleted
**PLATELET DISORDERS
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**Coagulopathy
+Causes of prolonged PT or PTT (prothrombin time or partial thromboplastin time) :
+Prolonged PT
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.factor 7 deficiency
.Vit K deficiency
.liver disease
.warfarin use
.factor 7 inhibitor
+Prolonged PTT
.vWf
.factor 8, 9, 11, 12 deficiency
.heparin
.antiphospholipid antibody
+Prolonged PT & PTT
.prothrombin, fibrinogen, factor 5, factor 10 or combined factor deficiency
.liver disease
.DIC
.supratherapeutic heparin or warfarin
.combined heparin and warfarin use
.direct thrombin inhibitors
.inhibitor of prothrombin, fibrinogen or factor 5, 10
*Hemophilia A and B
- The deficiency of factor 8 in hemophilia A and factor 9 in hemophilia B resulting in an increased risk of bleeding
-Signs & Symptoms :
.mild deficiencies (25% or greater activity) result in either the absence of symptoms or with symptoms only during surgical
procedures or with trauma
.more severe deficiency (<5-10% activity) can result is spontaneous bleeding
.type of bleeding found with factor deficiencies are (hemarthrosis, hematoma, gastrointestinal bleeding or urinary bleeding,
bruising and CNS bleeding may occur)
.severe hemophilia is obvious in most Pts by the age of two/ The disorder becomes apparent often at the time of circumcision
-Causes :
.both hemophilia A and B are x-linked recessive disorders resulting in disease in males
.females are carriers of the disease. Females do not express the disease because they would have to be homozygous, which is a
condition resulting in intrauterine death of the fetus hemophilia A is far more common than B
-Diagnosis :
.a prolonged PTT with a normal PT is expected
.a factor deficiency is strongly suspected when a 50:50 mixture of the Pts blood is created with a normal control and the PTT
drops to normal. This is known as a ‘mixing study’
.the mixing study will only tell you that a deficiency is present;it will not tell you which specific factor is deficient
.specific factor 8, 9 levels are necessary to determine a precise diagnosis. This is true of both hemophilia A and B
-Treatment :
.mild hemophilia can be treated with desmopressin DDAVP
.desmopressin can also be used prior to surgical procedures in mild hemophiliacs
.desmopressin works by releasing subendothelial stores of factor 8
.more severe deficiencies are treated with replacement of the specific factor
.desmopressin does not work for hemophilia B
*Vitamin K deficiency
-The deficiency of Vit K resulting in decreased production of factor 2, 7, 9 and 10
-Signs & Symptoms :
.bleeding may mimic that of hemophilia and may occur at any site. Look for oozing at venipuncture sites
-Causes :
.Vit K deficiency can be produced by dietary deficiency, malabsorption and the use of antibiotics that kill the bacteria in the
colon that produce Vit K
-Diagnosis :
.both Pt and PTT are elevates
.the PT usually elevates first and more severely
179
.a correction of the PT and PTT in response to giving Vit K is the most common method of confirming the diagnosis
-Treatment :
.severe bleeding is treated with infusions of fresh frozen plasma
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.Vit K is given at the same tome to correct the underlying production defect
*Liver Disease
-Coagulopathy from the decreased production of clotting factors by the liver
-Signs & Symptoms :
.bleeding may occur at any site, but the gastrointestinal tract is the most common site
-Causes :
.any severe liver disease or cirrhosis leads to a decreased production of the majority of clotting factors that are generally all
made in the liver, except for factor 8 and von willebrand factor. Factor 7 is first factor to be depleted
-Diagnosis :
.Pts. have an elevation of both PT and PTT, but the PT elevated first and is often more severely affected
.the disorder is clinically indistinguishable from Vit K deficiency except that there is no improvement when Vit K is given
.low platelet counts are often present from the hypersplenism that accompanies the liver disease
-Treatment :
.fresh frozen plasma is used acutely to correct severe bleeding such as melena
.long term management is based on the nature of the liver disease
**BLOOD TRANSFUSION
-Complications Of Blood Transfusion / Potential Risk :
.Hypothermia
.Hypocalcemia
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.Hyperkalemia
.Thrombocytopenia
.Hemolytic reactions
.Anaphylactic reactions
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.Hepatitis C
.HIV infection
.Acute congestive heart failure
.Transmission of infection
.Transfusion reaction
.Acidosis
.Impaired hemostasis
.Citrate toxicity
.Impaired oxygen delivery
.Incompatibility
.Noncardiogenic pulmonary edema
+The most fatal complication of blood transfusion is (Human error)
+Diseases Are Transmitted Through Blood Transfusion :
.Syphilis
.Malaria
.Hepatitis B and C
.Epstein-Barr virus
.Helicobacter Pylori (are NOT)
+In vascular injury the immediate response that produce hemostasis is (Vasoconstriction)
+Platelets normally have a half life of (7 days)
+In human being, normal red blood cell survival time is approximately (120 days)
+Generalized Increased Pigmentation May Be Seen In (skin) :
.Chronic liver disease
.Addison disease
.Hemochromatosis
.Ectopic ACTH secretion
.Nelson's syndrome
.Hemochromatosis
.Chronic renal failure
.Primary biliary cirrhosis
+Causes Of Hypopigmentation (skin) :
.Albinism
.Tuberous sclerosis
.Post inflammatory
.Vitiligo
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CARDIOLOGY
**Coronary Artery Disease (Atherosclerotic Heart Disease)
-Is a group of diseases that (Ischemic heart disease) :
.stable angina
.acute coronary syndromes (unstable angina, myocardial infarction, ST-segment elevation, non ST-segment elevation)
-Signs & Symptoms :
.typical chest pains
.retrosternal (central)
.heaviness (tightness)
.radiates to Lt. arm (or Lt. shoulder)
.pain aggravated by exertion
.pain relieved by rest
-Risk factors :
.smoking
.hypercholesterolemia (LDL)
.hypertension
.hyperglycemia (due to DM or otherwise)
.type A behavioural pattern
.lack of exercise
.stress
.alcohol, smoking
.obesity, diet rich in saturated fats (saturated fat – harmful / unsaturated fat – useful)
.men over 60; women over 65 (M > F) (in females – estrogen protect)
*Angina
1.Stable Angina
.is a classic type of angina related to myocardial ischemia
.a typical presentation of stable angina is that of chest discomfort and associated symptoms precipitated by some activity
(running, walking, etc.) / With minimal or non-existent symptoms at rest or after administration of sublingual nitroglycerin
2.Unstable Angina
.it occurs at rest (or with minimal exertion), usually lasting 3–5 minutes
.it is severe and of new onset (i.e., within the prior 4–6 weeks)
.it occurs with a crescendo pattern (distinctly more severe, prolonged, or frequent than before)
.is sometimes referred to as ‘preinfarction’ angina
-Diagnosis :
.ECG-electrocardiogram (normal or non-specific changes)
.cardiac enzymes (normal)
.exercise stress test (best test)/exercise ECG test “treadmill test” (stop it when – occur chest pain, ECG changes)
(contraindication – peripheral vascular disease, osteoarthritis, MI, unstable angina)
.cardiac catheterization (IS BEST)
-Treatment :
.Propranolol
.nitroglycerin (sublingual-at home)
.beta-blockers and calcium channel blockers (act to decrease the heart's workload)
.statins
.baby aspirin (100mg)
.stopping smoking
+In ER :
.O2
.nitroglycerin
182
.aspirin
+Side Effect Of Nitroglycerin :
.headache (M.C)
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.hypotension
+Contraindications (Nitroglycerin) :
.systolic Bp <90
.sildenafil (viagra) <24hrs
.phosphodiesterase 5-inhibitor
**Myocardial Infarction
*NSTEMI (non ST-segment elevation MI) (Heart Attack) Vs STEMI (ST-segment elevation MI)
-Is considered to have occurred if ischemia produces damage detectable by biochemical markers of myocardial injury (troponin
or CK-MB) / If there are no detectable serum markers of myocardial injury 12-18hrs after symptoms onset,the Pt should be
diagnosed with UA
-Signs & Symptoms :
.chest pain
.pain radiates most often to the Lt. arm, but may also radiate to the lower jaw, neck
.difficulty in breathing (shortness of breath-dyspnea)
.nausea, vomiting
.sweating
.palpitation
+Silent MI is M.C in the elderly in Pts. with DM (epigastric pain)
-Risk factors :
.high serum cholesterol level
.elevated low density lipoprotein level (LDL)
.hypertension
.DM
.smoking
.male gender
.obesity
.increasing age
.family history
.excess alcohol and carbohydrates intake
.stressful life-style
+Complications Of Myocardial Infarction :
.DVT
.heart arrhythmia (M.C.C of death in the 1st hr post-MI)
.acute & Chronic heart failure (congestive heart failure) (M.C.C of heart failure is ischemic heart disease)
.cardiogenic shock (massive MI / inferior MI)
.papillary muscle rupture (mitral regurgitation)
.dressler’s syndrome - pericarditis (2-6wks after MI)
.ventricular aneurysm, (2-3 days, persistent ST-elevation)
.thromboembolism
.myocardial rupture (>1wk from MI)
-Diagnosis :
1.ECG
.The usual ECG findings of NSTEMI are (ST-segment depression) or (T-wave inversion)
2.CARDIAC MARKERS (Cardiac Enzymes – BEST)
.Cardiac Specific isoenzyme CK-MB (creatine kinase myocardial band) (starts to rise at 4-6 hours and falls to normal within 48-72
hours)
.Cardio Specific proteins (troponin-T) and (troponin-I) are rises in blood in NSTEMI (Troponin-T and troponin-I start to rise at 4-6
hours and remain high for up to two weeks)
+If cardiac enzyme (-) repeat after 6hrs
+Lipids (LDL, HDL, Triglyceride (TG), Cholestrol)
3.FULL BLOOD COUNT
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5.ECHO
-Treatment :
+Oxygen, aspirin, morphine and nitroglycerin (are usually administered as soon as possible)
.baby aspirin (antiplatelet therapy)
.heparin (antithrombin therapy – anticoagulant)
.glycoprotein (GP) Iib/IIIA inhibitors
.beta-blocker
.intravenous nitroglycerin (NTG) for refractory pain
.CABG (coronary artery bypass graft)
+Patients With NSTEMI Have A :
.normal physical examination
.abnormal ECG
.particularly dynamic ST-segment deviation
.T-wave inversion
+Cardia Enzymes :
.troponin I (most specific -1st)
.CK-MB (2nd)
.AST
.LDH (lactate dehydrogenase)
+Causes False Positive Troponin :
.Septic shock
.Pulmonary embolism
.Pulmonary edema
.Renal failure
+Causes Increased In Troponin :
.Pulmonary edema
.MI
.Congestive heart failure
.Myocarditis
between heartbeats
-Complications :
.stroke
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.heart failure
.cardiac arrest
.sudden cardiac death
-Types :
.extra beats (premature atrial contractions and premature ventricular contractions)
.supraventricular tachycardias (atrial fibrillation, atrial flutter, and paroxysmal supraventricular tachycardia)
.ventricular arrhythmias (ventricular fibrillation and ventricular tachycardia)
.bradyarrhythmias
-Classifications :
+Atrial
.Sinus bradycardia
.Premature atrial contractions (PACs)
.Wandering atrial pacemaker
.Atrial tachycardia
.Multifocal atrial tachycardia
.Supraventricular tachycardia (SVT)
.Atrial flutter
.Atrial fibrillation (Afib)
+Junctional arrhythmias
.AV nodal reentrant tachycardia
.Junctional rhythm
.Junctional tachycardia
.Premature junctional contraction
+Ventricular
.Premature ventricular contractions (PVCs)
.Accelerated idioventricular rhythm
.Monomorphic ventricular tachycardia
.Polymorphic ventricular tachycardia
.Ventricular fibrillation
.Torsades de pointes
+Heart blocks
.These are also known as AV blocks, because the vast majority of them arise from pathology at the atrioventricular node. They
are the M.C.C of bradycardia :
.First degree heart block, which manifests as PR prolongation
.Second degree heart block
(Type 1 Second degree heart block, also known as Mobitz I or Wenckebach / Type 2 Second degree heart block, also known as
Mobitz II)
.Third degree heart block, also known as complete heart block
+Sudden arrhythmic death syndrome (SADS)
.is a term used as part of sudden unexpected death syndrome to describe sudden death due to cardiac arrest brought on by an
arrhythmia in the presence or absence of any structural heart disease on autopsy
.The M.C.C of sudden death is coronary artery disease specifically because of poor oxygenation of the heart muscle, that is
myocardial ischemia or a heart attack
-Causes of SADS in young people :
.viral myocarditis
.long QT syndrome
.Brugada syndrome
.Catecholaminergic polymorphic ventricular tachycardia
.hypertrophic cardiomyopathy
.arrhythmogenic right ventricular dysplasia
-Treatment :
.beta blockers or agents that attempt to restore a normal heart rhythm such as procainamide
.Amiodarone IV
.Diltiazem IV
+Antiarrhythmics Drugs:
185
.Xylocaine
.Quinidine
.Amiodarone
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.Procainamide
+Causes Of MI Without ACS (acute coronary syndrome) :
.protein C deficiency
.polycythemia vera
.thrombocytosis
.coronary spasm
.coronary artery embolus
.SLE
.polyarteritis nodus
.kawasaki
+Causes Of Tachycardia :
.Amphetamine
.Anemia
.Antiarrhythmic agents
.Atrial fibrillation
.Atrial flutter
.Atrial tachycardia
.AV nodal reentrant tachycardia
.Brugada syndrome
.Caffeine
.Cocaine
.Exercise
.Fear
.Fever
.Hypoglycemia
.Hypovolemia
.Hyperthyroidism
.Hyperventilation
.Infection
.Junctional tachycardia
.Multifocal atrial tachycardia
.Nicotine
.Pacemaker mediated
.Pain
.Pheochromocytoma
.Sinus tachycardia
.Wolff-Parkinson-White syndrome
+Causes Of Bradychardia :
.Obstructive jaundice
.Recreational drug use or abuse (digoxin)
.metabolic or endocrine issues, especially in the thyroid
.Electrolyte imbalance
.Neurological factors
.Autonomic reflexes
.Situational factors such as prolonged bed rest
.Autoimmunity
.Cardiac causes (acute or chronic ischemic heart disease, vascular heart disease, valvular heart disease, or degenerative primary
electrical disease)
+In general, two types of complications result in bradycardias :
.disorders of the sinoatrial node (SA node)
.disorders of the atrioventricular node (AV node)
.shortness of breath (worse with exercise, while lying down, and may wake the person at night)
.excessive tiredness
.leg swelling
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-Diagnosis :
.Echo
-Treatment :
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.angiotensin-converting enzyme (ACE) inhibitors (1st line therapy for all HF Pts.)
+ACE (enalapril, captopril, lisinopril, ramipril)
.angiotensin receptor blocker ARB (losartan, valsartan) (NO cough)
.beta-blockers (metoprolol, bisoprolol, carvedilol) (only this 3 drugs)
.digoxin (digitalis)
+Side effects of digoxin therapy :
.nausea, vomiting
.yellow vision
.AV block
.ventricular extrasystole
+Side effects of ACE-inhibitors :
.angioneurotic edema
.hyperkalemia
.dry cough
.hypotension
+Indications for the use of Beta-blockers :
.angina
.hypertension
.after myocardial infarction
.congestive heart failure CHF
.ischemic heart disease
.migraine
.anxiety
+Crepitations which are late inspiratory and unchanged with cough are typical of Pulmonary edema
**Hypertension HTN
-Normal Bp at rest is within the range of (100-140 mmHg systolic – top reading / 60-90 mmHg diastolic – bottom reading)
-Types :
.primary hypertension (90-95% of cases) (M.C)
.secondary hypertension (5-10% of cases)
-Causes Of Primary Hypertension :
.is rarely accompanied by any symptoms (and its identification is usually through screening)
-Causes Of Secondary Hypertension :
.Renovascular hypertension – Renal Artery Stenosis (M.C.C) (Fibromuscular dysplasia – in young females / Atheromatous
stenosis – in old age Pts.)
.Hypertension secondary to renal disorders (CRF / Glomerulonephritis)
.Hypertension secondary to endocrine disorders (Pheochromocytoma – caused by an excessive secretion of norepinephrine
and epinephrine which promotes vasoconstriction / Hyperaldosteronism – Conn's syndrome / Cushing`s syndrome – an
excessive secretion of glucocorticoids causes the hypertension / Hyperparathyroidism / Hyperthyroidism – systolic HTN /
Hypothyroidism – diastolic HTN / Acromegaly)
.Hypertension Secondary To Other Causes (Pregnancy, Drugs, Liquorice, Coarctation Of Aorta)
-Complications :
.MI
.stroke
.left ventricular hypertrophy
.hypertensive cardiomyopathy
.hypertensive encephalopathy
.hypertensive retinopathy
.hypertensive nephropathy
-Treatment :
.diuretics (1st drug is thiazide)
.beta-blockers (atenolol, metoprolol, propranolol) (post MI)
.mixed (alpha + beta-blocker ‘labetalol’) (in pregnancy)
.alpha-blockers (tamsulosin, doxazosin, alfuzosin) (pregnancy)
.ACE inhibitors (captopril, enalapril) (for heart failure)
188
**Infective Endocarditis
-Inflammation, of the inner tissue of the heart, such as its valves
+M.C bacteria-Organism in infective endocarditis is (Streptococcus Viridans)
+M.C bacteria in I.V drugs abusers is (Staphylococcus Aureus)
+The site of endocarditis in drug abusers is (Tricuspid Valve)
+M.C bacteria in prosthetic valve is (Staphylococcus Epidermidis)
189
.fever
.clubbing
.weight loss
.heart murmur
.roth's spots (on the retina)
.Osler's nodes (painful subcutaneous lesions in the distal fingers)
.janeway lesions (painless hemorrhagic cutaneous lesions on the palms and soles)
.intracranial hemorrhage
.conjunctival hemorrhage
.splinter hemorrhage (nail hemorrhage)
.renal infarcts
.splenic infarcts or splenomegaly
.vascular phenomena (septic embolism – causing thromboembolic problems such as stroke in parietal lobe of the brain or
gangrene of fingers
.anemia
.malaise
.fatigue
.hematuria
.anorexia
-Causes :
.bacteremia (Streptococcus viridans, Staphylococcus aureus)
+Bacteremia caused by (dental procedures and I.V drug abusers)
-Classifications :
.subacute bacterial endocarditis SBE (M.C is Streptococcus viridans)
.acute bacterial endocarditis ABE (M.C is Staphylococcus aureus)
-Diagnosis :
+Major criteria include :
.positive blood culture
.positive echo + vegetation
+Minor criteria include :
.predisposing factor (known cardiac lesion, recreating drug injection)
.fever >38c
.evidence of embolism (arterial emboli, pulmonary infarcts, janeway lesions, conjunctival hemorrhage)
.immunological problems (glomerulonephritis, Osler`s nodes)
-Treatment :
.high dose antibiotics (2-6 weeks)
+Fever Of Unknown Origin :
.Infectious (endocarditis, TB, Brucella, Typhoid, Malaria)
.Malignancy (leukemia, lymphoma)
**Rheumatic Fever
-Is an inflammatory disease that occurs following a Streptococcus pyogenes infection caused by antibody cross-reactivity that
can involve the heart, joints, skin, and brain
+The disease typically develops 2-4 weeks after a throat infection (occur post-Streptococcal infection - tonsillitis)
+Acute rheumatic fever commonly appears in children between the ages of 6-15 age
-Signs & Symptoms :
+Major Criteria
.polyarthritis, arthritis
.carditis
.erythema marginatum (itchy rash)
.sydenham's chorea
.subcutaneous nodules
+Minor Criteria
.fever
.arthralgia
190
.raised ESR
.C-reactive protein, leukocytosis, WBS elevated
.erythema nodosum
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+Others
.multiple painful joints
.involuntary muscle movements
.atrial fibrillation
.infection of the valves
.abdominal pain
.nose bleeds
-Diagnosis :
.evidence (Anti-streptolysin O - ASO or ASLO) + 2 major criteria, OR
.evidence (ASO titer + 1 major + 2 minor), OR
.evidence (ASO titer + Chorea)
+Chorea - a neurological disorder characterized by jerky involuntary movements affecting especially the shoulders, hips, and
face
-Treatment :
.high dose antibiotics (pencillin)
.NSAID (Aspirin)
.erythromycin, prednisone
+Lipid lowering agents :
.statine
.fibrates (gemafibrozil)
.bile acid binding
.nicotinic acid
.fish oil (omega-3)
**Syncope
-Is defined as a short loss of consciousness and muscle strength, characterized by a fast onset, short duration and spontaneous
recovery
-Cardiac Syncope (is sudden without warning and complete recovery / last for 1-2min)
-Causes of cardiac syncope :
.arrhythmia (bradycardia and tachycardia)
.obstructive cardiac lesion (Aortic stenosis and mitral stenosis)
.acute aortic dissection
.pericardial tamponade
.pulmonary embolism
.pulmonary hypertension.
.hypertrophic cardiomyopathy
.idiopathic
.hyperthyroidism
.pneumonia
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.pericarditis
.cardiac surgery
.alcohol
.congenital heart disease
+Wolf Parkinson White Syndrome (WPW) :
.ECG (delta wave)
.usually associated with atrial fibrillation
.drug to choice is (amiodarone)
+Atrial Flutter :
.ECG (saw-tooth appearance)
.management like atrial fibrillation
+Homocystinuria + Lipoproteinemia (risk factor for IHD)
+Lipoproteinemia - A disorder in which the proteins that carry fat around the body are defective
+Homocystinuria - It is an inherited autosomal recessive trait, which means a child needs to inherit a copy of the defective gene
from both parents to be affected (is an inherited disorder of the metabolism of the amino acid methionine, often involving
cystathionine beta synthase)
**Pulmonary Edema
-Signs & Symptoms :
.dyspnea
.wheezing
.tachycardia
.cyanosis
.cough with expectoration (pink frothy sputum)
.gallop rhythm
.crackles
-Causes :
.Lt. sided HF (M.C)
.MI
.mitral regurgitation
.mitral stenosis
.aortic regurgitation
.arrhythmia
+Pulmonary edema is caused by :
.Fallot Tetralogy
.Acute glomerulonephritis
.Aspiration of hydrocarbons
.Left to right shunt
-Diagnosis :
.CXR (bilateral shadow - butterfly)
.Kerley B lines
-Treatment :
.Pt. in sitting position
.oxygen (60%)
.furosemide I.V (40-80%)
.morphin
.aminophylline
.C-PAP
.pulmonary edema
.hemoptysis
.hoarseness of voice
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.malar flush
.diastolic murmur (loud S1)
.thromboembolism + atrial fibrillation
.opening snap (S2)
.pre-systolic murmur
.rumbling mid-diastolic murmur
.dyspnea, orthopnea
.systemic embolism
.Rt. sided heart failure (hepatomegaly, ascites, peripheral edema)
-Causes :
.rheumatic fever (M.C.C)
.rheumatic heart disease
.calcification
.CHD
.mitral valve (it is the most common valvular heart disease in pregnancy)
.infective endocarditis
.endomyocardial fibroelastosis
.malignant carcinoid syndrome
.systemic lupus erythematosus
.whipple disease
.fabry disease
.rheumatoid arthritis
.hurler' disease
.hunter's disease
.amyloidosis
*Mitral Regurgitation
+The symptoms associated with MI / F > M
-Signs & Symptoms :
.congestive heart failure (shortness of breath, pulmonary edema, orthopnea, and paroxysmal nocturnal dyspnea)
.symptoms of cardiogenic shock (shortness of breath at rest)
.cardiovascular collapse with shock (cardiogenic shock)
.infective endocarditis of the mitral valve
.holosystolic murmur
.loud S3
.tachycardia
-Causes :
.rheumatic fever (M.C.C)
.Marfan's syndrome
.hyperthyroidism
.mitral valve prolapse (MVP)
.myxomatous degeneration
.Ehlers Danlos Syndrome
.Ischemic heart disease
.chordae tendineae
.pulmonary edema
.Lt. atrial enlargement
.pansystolic murmur (late systolic click)
+Rheumatic heart disease affects most commonly Mitral valve
.loud S3
-Causes :
.pulmonary hypertension
.Rt. ventricular dilation (right ventricular infarction, inferior myocardial infarction, and cor pulmonale)
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.endocarditis
.pulsatile liver
.increased JVP
.rheumatic
.myxomatous
.ebstein anomaly
.endomyocardial fibrosis
.traumatic (blunt chest injury)
.LV dysfunction or valve disease
.chronic lung disease
.pulmonary thromboembolism
.RV ischemia
.Left to right shunt
*Aortic Regurgitation
-Can cause pulmonary edema
-Signs & Symptoms :
.causes wide pulse pressure
.head nodding
.collapsing pulse
.diastolic murmur
.pulse pressure (systolic increased-diastolic decreased)
.left ventricular impulse
.pistol shot femoral pulses
**Cardiomyopathy
-"heart muscle disease" is the measurable deterioration for any reason of the ability of the myocardium (the heart muscle) to
contract, usually leading to heart failure
-Signs & Symptoms :
.dyspnea
.peripheral edema
.irregular heart rate
.sudden cardiac death
-Types :
1.Dilated Cardiomyopathy DCM
.is a condition in which the heart becomes enlarged and cannot pump blood efficiently (M.C form)
194
(thickened) without any obvious cause, creating functional impairment of the cardiac muscle
.familial (autosomal dominant)
.M.C.C of sudden death in young athletes
3.Restrictive Cardiomyopathy RCM
.is a form of cardiomyopathy in which the walls are rigid, and the heart is restricted from stretching and filling with blood
properly
.M.C.C is amyloidosis
4.Constrictive Pericarditis
.is a medical condition characterized by a thickened, fibrotic pericardium, limiting the hearts ability to function normally
.M.C.C is idiopathic
-Other Causes :
.TB
.sarcoidosis
.Rt. side heart failure
.lower limbs edema
.ascites
.hepatomegaly
.chronic renal failure
.post-myocardial infection
.post-viral pericarditis
.chronic pericarditis
.heart surgery
+Contraindication for thrombolytic therapy :
.stroke (within 2 months)
.HTN (uncontrolled)
.surgery (within 6 days)
.bleeding disorder
.non-STEMI
.post MI (>12hrs)