Abu Gharbieh's Capsule Lecture Notes in Medicine

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Abu Gharbieh's Capsule
Lecture Notes In
Medicine
Yazan Abd Al-majed Abu Gharbieh
Abu Gharbieh's Capsule

Lecture Notes In
Medicine
‫المملكة األردنية الهاشمية‬
‫رقم اإليداع لدى دائرة‬
‫المكتبة الوطنية‬
‫( ‪)2020/3/1025‬‬
‫‪616.3‬‬
‫‪Abu Gharbieh, Yazan A.Hashem‬‬
‫‪Abu Gharbieh's Capsule Internal Medicine /‬‬

‫‪Yazan A.Hashem Abu Gharbieh .-Amman: The Author,‬‬
‫‪2020‬‬
‫‪( ) p.‬‬
‫‪Deposit No.: 2020/3/1025‬‬
‫‪Descriptors:/Internal Disease//internal Medicine//‬‬
‫‪Medicine /‬‬
‫يتحمل المؤلف كامل المسؤولية القانونية عن محتوى مصنفه وال يعبر‬
‫هذا المصنف عن رأي دائرة المكتبة الوطنية أو أي جهة حكومية أخرى‪.‬‬
‫جميع حقوق التأليف والطبع والنشر محفوظة‬
‫ال يجوز بيع أو نشر أو اقتباس أو التطبيق العملي أو النظري ألي جزء أو فكرة‬
‫من هذا الكتاب أو اختزان مادته بطريقة االسترجاع‪ ،‬أو نقله على أي وجه‪ ،‬أو‬
‫بأي طريقة‪ ،‬سواء أكانت إلكترونية أو ميكانيكية‪ ،‬أو بالتصوير‪ ،‬أو بالتسجيل‪ ،‬أو‬
‫بخالف ذلك‪ ،‬دون الحصول على إذن الناشر الخطي وبخالف ذلك يتعرض‬
‫الفاعل للمالحقة القانونية والقضائية‪.‬‬
introduction :
The book is a review on the various internal medicine topics that are
tested in the medical examination for the candidates preparing for
Jordan medical council exam ( license exam ), medical students
exams and residency acceptance exams in ministry of health of
Jordan , Royal medical services and different Jordanian hospitals.
I am glad to offer my expertise and knowledge that I had

accumulated over time and by using many highly-yield textbooks like:
1) Kaplan STEP 2 CK Leture Notes
2) Davidson’s Essential of Medicine
I hope you find this book useful in your everyday practice and in
preparation for your professional examinations to get top scores and
hopefully leave a strong and lasting imprint in your minds.
Yazan Abu Gharbieh
: ‫المقدمة‬
‫الكتاب يعتبر كمراجعة لمادة طب الباطني للمتقدمين المتحانات المجلس الطبي االردني ( امتحان‬
‫ الخدمات‬, ‫ امتحانات كليات الطب و امتحانات القبول لبرامج االقامة في وزارة الصحة‬, (‫المزاولة‬
. ‫الطبية الملكية وغيرها من المستشفيات االردنية‬
‫ كما قمت باالستعانه ببعض‬, ‫لقد وضعت خبرتي ومعرفتي التي جمعتها طول الوقت في هذا الكتاب‬
:‫المراجع الطبيه العالميه ومنها‬
1) Kaplan STEP 2 CK Leture Notes
2) Davidson’s Essential of Medicine
‫اتمنى ان تجدوا هذا الكتاب مساعدا لكم في ممارستكم الطبية وفي التحضير المتحانتكم للحصول‬
. ‫على اعلى الدرجات و اتمنى ان اكون تاركا ً بصمة قوية ودائمة في ذاكرتكم‬
‫يزن ابو غربية‬

Chapter 1: Endocrinology
1
Chapter 2: Rheumatology
35
Chapter 3: Gastroenterology
55
Chapter 4 : Cardiology
83
Chapter 5 : Hematology
127
Chapter 6: Infectious Disease

157
Chapter 7 : Nephrology
197
Chapter 8: Pulmonology
231
Chapter 9: Emergency Medicine

257
Chapter 10: Neurology

283
The Most common

311
Normal Values
317
Chapter 1
Endocrinology
Pituitary gland
1- Pituitary is surrounded by sphenoid bone

2- Covered by sellar diaphragm (extension of dura matter)
3- It lies in the sella turcica underneath the optic chiasm.
4- It is 2 lobes: 1- posterior lobes (neurohypophysis): storage site for hormones
produced by supraoptic & paraventricular nucleus > ADH, oxytocin.
2- Anterior lobe (adenohypophysis): 80% of pituitary produces: GH,
prolactin, TSH, ACTH, LH, FSH.
5- Anterior pituitary hormones are regulated by releasing & inhibiting hormones
from hypothalamus.
DISEASES OF THE ANTERIOR PITUITARY

- Microadenomas tumors < 1𝑐𝑚 𝑖𝑛 𝑑𝑖𝑎𝑚𝑒𝑡𝑒𝑟
- Macroadenomas tumors > 1𝑐𝑚 𝑖𝑛 𝑑𝑖𝑎𝑚𝑒𝑡𝑒𝑟
Hyperprolactinemia.
Etiology:
1- physiological : Pregnancy, early nursing, sleeps, exercise, Hypoglycemia,

seizures, stress, nipple stimulation
2- liver Cirrhosis, Chronic Renal Failure.
3- Adenomas: Microadenomas > women
Macroadenomas > men + visual defects
4- CNS tumor : craniopharyngioma, meningioma, dysgerminoma
5- Drugs: phenothiazines, metoclopramide & methyldopa, reserpine, TCA,
NARCOTICS, COCAINE, SSRI, Risperidone, verampile
6- Hypothyroidism
0795407665 ‫الدكتور يزن ابو غربيه‬

1
Clinical Pictures:
1- Women: galactorrhea, menstrual abnormalities amenorrhea, oligomenorrhea,

osteopenia, osteoporosis, Infertility, gynecomastia.
2- Men: hypogonadism, erectile dysfunction, decrease libido, gynecomostia,

Infertility.
Diagnosis: 1- Pregnancy test 2- Check medications 3- TFT 4- KFT 5- LFT 6-

prolactin level (>100 ng/ml) 7- MRI
Management:
1- dopamine agonist: bromocriptine, cabergoline

2- surgery If no response to medication
3- Radiation if fail medication and surgery
Acromegaly:
In children called gigantism.
Etiology: 1- Macroadenomas : most common cause
2- ectopic tumor
produce GH or GHRH
Clinical Findings:
1- Skeletal soft tissue changes.

2- Enlargement, hands & feet,
coarsening of facial features,
thickened skin folds > Increase
in show, glove, hat, ring
3- Nose, mandible enlarge
(prognathism)
4- sweating
5- obstructive sleep apnea
6- internal organ enlarged: heart,
lung
7- Menstrual problems.
8- HTN, arrhythmias, HCM,
DM.
9- Interstitial edema, entrapment
neuropathy Carpal tunnel
syndrome

2
Diagnosis:
1- IGF = Initial test
2- GH after 100g glucose = most accurate
3- CT, MRI After level of hormone
Treatment:
1- Surgery: Primary treatment
2- Dopamine agonists: bromocriptine, cabergoline
3- octreotide (somatostatin analogues) best medical therapy>> side effect:
cholestasis, cholecystitis
4- pegvisomant: GH analogue blocking binding GH to its receptor in liver
5- Radiation
Complications: Heart Failure (most common of Death)
DM, cord compression, visual field defects.
Hypopituitarism.
- Partial or complete loss of anterior pituitary
- First hormone to be lost FSH, LH, GH > TSH > ACTH
Etiology:
1- Tumor of pituitary or hypothalamus (craniopharyngioma, meningioma, gliomas)
adenoma most common.
2- Pituitary apoplexy: is syndrome with acute hemorrhagic infarction of preexisting
adenoma (emergency) > headache, nausea, vomiting, depression of
consciousness.
3- Inflammatory disease (sarcoidosis, TB, Syphilis)
4- Trauma, radiation, surgery - hypoxia.
5- Vascular: Sheehan postpartum necrosis (first sign: no lactation)
6- Infiltrative disease. hemochromatosis, amyloidosis
7- stroke
Clinical picture:
1- LH & FSH: women >> amenorrhea, genital atrophy, infertility and decrease libido,
loss of axillary & pubic hair
Men >> impotence, testicular atrophy, infertility and decrease libido, loss of auxiliary
& pubic hair
2- GH: Fine wrinkles, hypoglycemia, high level lipid, low (muscle, bone, heart )
mass.
3- TSH: hypothyroidism: Fatigue, weakness hyperlipidemia, cold intolerance, puffy
skin

3
4- ACTH: 2ND Adrenal insufficiency

5- cortisol: Fatigue, low appetite, weight loss, skin and nipple pigment, low response
to stress.
Diagnosis:
1- GH: Insulin - induced hypoglycemia test, arginine test
2- ACTH: give basal cortisol then do insulin tolerance test or metyrapone test or
cosyntropin
3- Gonadotropin: women >> LH,FSH,estrogen
Men >> LH, FSH, testosterone
4- TSH: TSH, T4, T3
Treatment:
1- treating underlying cause.
2- hormone Replacement start with cortisol
Empty sella syndrome (ESS)
- herniation of supracellar subarachnoid space through incomplete diaphragm

- Most common in multiparous women
- No pituitary on CT, MRI
- Treatment: is reassurance.
DISEASES OF THE POSTERIOR PITUITARY.

Central & nephrogenic Diabetes Insipidus.
Etiology
1- Central: any cause of pituitary or hypothalamus adenomas, craniopharyngiomas,
head injuries, HTN, meningitis
2- nephrognic: hyper Ca, hypo k, SSC, amyloidosis, sjogren's syndrome. Drugs:
(lithium, demeclocycline, colchicines)
Clinical pictures:
1- Polyuria, excessive thirst
2- Polydipsia (16-20L/d)
3- Nocturia
Diagnosis
1- Labs: hyper NA + high serum osmolarity + low urine osmolarity & specific
gravity
2- Water deprivation test
3- ADH level
Differential Diagnosis

4
1- Psychogenic polydipsia
2- Drug induced polydipsia (chlorpromazine thioridazine, anticholinergic)
3- hypothalamic disease
Management:
Central:
1- hormone Replacement vasopressin, desmopressin

2- drug stimulate ADH: chlorpropamide, clofibrate, carbamazepine
Nephrogenic:
1- HCTZ, amiloride
2- Chlorthalidone
3- NSAID.
Syndrome of Inappropriate secretion of ADH
Etiology:
1- malignancies: small cell CA & pancreas CA.
2- Nonmalignant: TB, pneumonia, lung abscess
3- CNS: head injuries, CVA, encephalitis
4- Drug: chlorpropamide, clofibrate, carbamazepine, cyclophosphamide.
Clinical Pictures:
1- water retention without edema or HTN
2- Symptoms of hypoNa: Irritability, confusion, seizures, coma
Diagnosis: 1- Hyponotremia < 130𝑚𝐸𝑞/ 𝐿 2-Posm < 276 𝑚𝑜𝑠𝑚/𝑘𝑔

3- UNa > 20 𝑚𝐸𝑞/𝐿 4- low BUN, Creatinine, uric acid, albumin
Treatment:
1- Treat underlying causes
2- Fluid Restriction 800 -1000ml /d
3- Demeclocycline: inhibits ADH
4- V2 receptor blocker: conivapton, tolvaptan
5- Hypertonic saline: Rate of correction 0.5- 1 mmol/L/H

5
Thyroid Gland

6
Laboratory test in thyroid:

1- TSH: most sensitive
2- T4, T3 free reflect the function of thyroid not total T3, total T4.
3- High total T4 in pregnancy and OCP Low total T4 in nephrotic syndrome and
androgens
4- RAIU: increase in graves, toxic nodule, decrease in thyroiditis or ingestion
thyroid hormone
5- Antibodies: antithyroglobulin + antimicrosomal Ab > Hashimoto's... TSI Ab>
Graves
Hyperthyroidism
1- Drug: amiodarone, alpha interferon, lithium, contrast agents

2- Graves: hyperthyroidism+ diffuse goiter+ exophthalmus + dermopathy (pretibial
myxedema) (most common cause)
Pathology of Graves: TSI antibodies stimulates TSH Receptor.
- more common in female < 50 years
- dermopathy: it is area well demarcated raised thickened may be pruritic and
hyperpigmented
- Graves disease may be associated with other systemic autoimmune disease
such as: pernicious anemia, myasthenia graves, DM
- Eye disease is treated with steroid or radiation
- Skin disease is treated with steroids
3- Toxic nodule: can result from plummer

disease which is nonautimmune disease
common in elderly with arrhythmia + CHF
4- Transient Hyperthyroidism: subacute
thyroiditis, lymphocytic thyroiditis
5- Extrathyroid source: thyrotoxicosis factitia, ectopic thyroid tissue & struma ovarii
Clinical pictures:
1- A- FIB 2- emotional lability 3- Inability to sleep 4-tremors 5- frequent
bowel movements 6- Sweating 7- heat intolerance, weight loss 9-palpitation
10- angina 11- moist warm skin 12- palmar erythema 13- menstrual irregularity
14- infrequent blinking + lid lag
Diagnosis:
1- TSH: low in primary … high in secondary

2- High Free T4, T3
7
3- RIAU increase in graves

4- TSI antibodies in Graves
Treatment:
1- antithyroid drugs:
- methimazole :drug of choice due to longer half life, more quickly, fewer side effect
(less hepatotoxicity)
- propylthiouracil: drug of choice in pregnant in first trimester then switch to
methimazole for rest of pregnancy and nursing
- both drug cause agranulocytosis
2- radioactive iodine ablation indication:
- large thyroid gland
- multiple symptoms of thyrotoxicosis
- high thyroxine
- high titers of TSI
side effect: hypothyroidism >>will need thyroid replacement after that
3- Subtotal thyroidectomy for pregnant in 2nd trimester + children + compressive
symptoms
4- B B: propranolol to control symptoms
Note: antithyroid drug should be stopped 2 weeks before and after RAI because they
block uptake of radioactive iodine
Thyroid storm
- endocrine emergency: (extreme thyrotoxicosis)
- Etiology: stress, infection, surgery, trauma
Clinical picture: irritability, delirium, coma, tachycardia, restlessness, vomiting,

jaundice, diarrhea, Hypotension dehydration, fever
Treatment:
1- supportive: NLS + Glucose + glucocorticoids
2- O2 cooling blanket
3- Antithyroid drug
4- Iodine inhibit hormone release (wolff –Chaikoff effect)
5- - B B
6- Dexamethasone inhibit hormone release, impair peripheral generation of T3,
adrenal support

8
Hypothyroidism
Etiology:
1- Hashmioto disease: most common cause
2- Postablative surgery or radioactive iodine
3- heritable biosynthetic defects
4- Iodine deficiency
5- Drug: lithium, acetylsalicylic, Amiodarone, sulfonamides, interferon
Clinical Findings:
1- Newborn (cretinism): persistent physiologic jaundice, hoarse cry, constipation,
somnolence feeding problems, delayed milestones, dwarfism coarse features,
protruding tongue, Broad Flat nose, widely set eyes, sparse hair, dry skin, protuberant
abdomen, umbilical hernia, impaired mental development, retarded bone age, delayed
dentition
2- adult: lethargy, constipation, cold intolerance, stiffness & cramping of muscles,

carpal tunnel syndrome, menorrhagia, slow motor activity, decrease appetite, weight
increase, hair & skin dry, deep voice, deafness, slow motor reflexes, high cholesterol,
periorbital puffiness, large tongue, pale cool skin
Carpal tunnel syndrome: compression

of median nerve >> paraesthesia in
lateral 3digits causes:
1- Idiopathic: most common cause

2- RA
3- Hypothyroidism
4- pregnancy
5- amyloidosis
6- DM
7- acromegaly
8- obesity
Diagnosis:

9
Managment:
1- levothyroxine (T4):Should be monitored TSH/ T3 (it takes 6 weeks to stabilize.

2- Levothyroxine taken on empty stomach without any drug or multivitamins (Ca,
iron)
3- If there is suspicion of suprathyroid. hypothyroidism give hydrocortisone.
4- In pregnant: increase demand need close follow up start 4-6 weeks gestation then
every 4-6 week until 20 week
Myxedema coma
Etiology: Long standing hypothyroidism with precipitating factor
- Cold exposure, trauma, infections, CNS depressants.
Clinical pictures: hypothermic, stuporous state, respiratory depression
Treatment: High dose T4, T3
Thyroiditis:
1- Subacute Thyroiditis: (giant cell, de quervain)
Etiology: Viral origin follows upper respiratory Infection.
Clinical pictures: malaise, fever, pain over thyroid referred to lower jaw, ear: firm _
enlarged thyroid gland.
Diagnosis:
1- high ESR
2- decrease RAIU
3- high T3, T4 then low
Treatment: NSAID, Prednisone, propranolol
2- Hashimoto thyroiditis:
Etiology: autoimmune factor with lymphocytic infiltration.
Clinical pictures:
1- painless goiter
2- Rubbery not symmetrical gland.
3- Hypothyroidism
Diagnosis:
1- High TSH

10
2- Low T4, T3
3- antimicrosomal & antithyroperoxidase antibodies
Treatment: L- thyroxine
3- Lymphocytic (silent, painless, postpartum)
Etiology: unclear (lymphocytic thyroiditis)
Clinical pictures:
1- nontender Firm, Symmetrical slightly enlarged gland.

2- Hyperthyroidism
Diagnosis:
1- High T3, T4
2- Low RAIU
3- NORMAL ESR
Treatment: last for 2-5 month may recurrent & symptomatic treatment: propanolol
4- Reidel Thyroiditis: intense Fibrosis of thyroid & surrounding structures
Neoplasia of the thyroid
1-Papillary carcinoma:
1- Most common thyroid CA (70- 60%)

2- Most common in women
3- Spreads by lymphatics
4- Psammoma bodies microscopically
5- Treatment: small: surgery ….Large: surgery + Radiation
2-Follicular carcinoma:
1- Most common in elderly + women

2- Spread by blood.
3- not diagnosed with FNA because we need to evaluate capsular and vascular
invasion
4- treatment: surgery + Radiation
3- Anaplastic carcinoma:
1- in elderly patients
2- Highly malignant with Rapid & Painful enlargement.
11
3- Spread by direct extension

4- Most Patients die within 1 year.
4-Medullary carcinoma:
1- arises from parafollicular cell of thyroid

2- Produces calcitonin
3- component of Men IIA, MEN IIB
4- Treatment: surgery.
When to suspect thyroid CA:

1- Recent growth of thyroid or mass
2- history of Radiation therapy of head,
neck, in childhood.
3- Presence solitary nodule
4- Production of calcitonin
5- calcification on X ray
6- Psammoma approach to solitary
nonfunctioning nodule
Diagnostic approach to solitary nonfunctioning nodule
- TSH > FNA > radionuclide scan > U/S.
PARATHYROD GLANDS
- calcium regulation: by 3 hormones & 3 tissue\
- 3 tissue: bone, kidney, intestine.
- 3 hormones:
1. PTH (hyperca)
2. calcitonin (hypoca)
3. Vitamin D (hyperca)
Ca
98% bone 2% blood
50% free 40%protein 10% PO4 + citrate

12
Hypercalcemia:
Etiology:
1- primary hyperparathyroidism (most common cause)
2- Malignancy: PTH like protein
3- Granulomatous disease: sarcoidosis, TB, berylliosis, histoplasmosis (neutrophils
>> vitamin 25-vit D hydroxylation >> 1,25 vit D)
4- Vitamin D intoxication,
5- thiazides, lithium 6- paget disease 7- hyperthyroidism: stimulate osteoclast
8- acidosis 9- prolonged immobilization
10- Familial hypocalciuric hypercalcemia:
-mutataion of CaSR gene >> encodes Ca sensing receptor
- lead to high PTH
- hyperCa + hypocalciuria
- no treatment

13
Clinical picture
1- CNS: Coma, confusion, convulsions

2- GIT: constipation, anorexia, nausea, vomiting, pancreatitis, ulcer disease
3- Renal: polyuria, polydipsia, nephrogenic diabetes insipidus, kidney stones
4- CVS: HTN, ECG >> SHORT QT.
Treatment: 1- normal saline + furosemide
2- IV bisphosphonates: zoledronate, pamidronate >> inhibit osteoclast &

stimulate osteoblast
3- calcitonin: inhibits osteoclasts.
primary hyperparathyroidism
Etiology:
1- one gland adenoma (most common)

2- four gland hyperplasia
3- parathyroid cancer
4- men I, men IIA
Clinical pictures:
1- asymptomatic half of patients

2- osteitis fibrosa cystic: bone pain, fractures, swelling,deformity ,area of
demineralization, bone cyst,brown tumor (salt & paper appearance),manifestation of
hyperca (cns, GIT, nephro, cvs)
Diagnosis:
1- high PTH
2- high ca > 10.5 𝑚𝑔/𝑑𝑙
3- low PO4 < 2.5 𝑚𝑔/𝑑𝑙
4- nuclear parathyroid scan (sestamibi) to localize adenoma
Treatment:
1- reduce dietary CA 400 MG/DL
2- oral hydration 2-3L
3- phosphate supplementation, phospho soda
4- Parathyroidectomy: Indication
1- Symptomatic hyperca 2- ca >11.5 mg/dl

3- Renal insufficiency 4- age <50 years 5- Nephrolithiasis 6- osteoporosis

14
Emergency treatment for severe hyperca
1- Iv normal saline + furosemide

2- Iv bisphosphates
Note: Hungry bones syndrome:
hypocalcemia after surgical removal of hyperactive parathyroid gland(increase

osteoblast activity) decrease of calcium, phosphate, magnesium, 1-4 week post-
parathyroidectomy
Primary Secondary
Tertiary pseudohypoparathyr
hyperparathyr hyperparathyroid
hyperparathyroidism oidism
oidism ism
Failure of target cell
to response of PTH
Hypocalcemia: (genetic)
Parathyroid
Etiology vit D deficiency, Long –term secondary Sign: short 4th, 5th
adenoma
chronic kidney hyperparathyroidism metacarpals
disease Short stature
Round face
Mental retardation
Ca High Low High low
Variable (according to
Po4 Low Low normal
KFT)
Hypocalcemia
Etiology:
1- hypoparathyroidism (most common)

2- renal failure
3- hyperphosphatemia
4- hypomagnesemia
5- drug: loop diuretics, phenytonin, alendronate, foscarnet
6- alkalosis
7- low albumin (pseudo hypoCa)
8- massive blood transfusion.
Clinical finding:
1- hyperexcitability: seizure, tetany, cirumoral numbness tingling of the extremities
2- arrhythmias, prolonged QT,
3- Cataracts
Treatment: IV, oral calcium + vitamin D
Hypoparathyroidism
Etiology: 1- surgical Removal of thyroid. (most common cause)

15
2- hypomagnesemia 3- hereditary
Clinical finding:
1- Neuromuscular irritability tetany, laryngospasm, cramping, seizures impaired
memory function
2- chvostek sign
3- trousseau sigh
4- cataracts
5- soft tissue calcifications
6- QT prolongation.
Diagnosis:
1- Low Ca
2- check albumin (for pseudo hypoCa)
3- Low PTH
Treatment:
1- ca gluconate IV
2- oral calcium 2- 4g/d
3- vitamin D
4- diet restriction
5- phosphate binder (CaCo3, aluminuim hydroxide)
DIABETES MELLITUS
definition: disorder of carbohydrate metabolism caused by relative or absolute
deficiency of insulin, hyperglycemia, end-organ complication: nephropathy,
retinopathy, neuropathy
atherosclerosis
Classification:
1- type I (IDDM)
- autoantibodies to Islet cell
- associated with HLA-B8, HLA-
B15, HLA-DR3, HLADR4
- Patient lean body build prone to ketosis.
2- Type II (NIDDM)
- Age of 40 years
- > 20% of first degree relative
- Insulin resistant
- most common type
- Obese patient
Clinical findings:
1- hyperglycemia 2- polyuria, 3-polydipsia 4- polyphagia 5- Acute metabolic
decomposition (DKA, HONK)

16
Diagnosis:
1- glucose > 200 + symptoms
2- FBS ≥ 126 MG/DL in two occasionas
3- glucose ≥ 200mg/dl 2 hour after meal : oral glucose tolerance test
4- Hab1c ≥ 6.5%
Management
1- Non- pharmacologic treatment

1- Patient education 2- weight loss 3- low fat 4- physical activity
2- Pharmacological treatment after failure diet & exercise
I- Oral hypoglycemics: for all type 2
A- Metformin: first drag of choice in all newly diagnosed

- Not cause hypoglycemia
- not cause weight gain
- contraindicated in renal insufficiency
-side effect : nasue & diarrhea (most common) lactic acidosis
B- Sulfonylureas (glyburide, glipizide, glimepiride)

- Increase weight
- cause hypoglycemia
- Sulfa group
- side effect : hepatotoxicity
C- thiazolidinediones (Rosiglitazone, pioglitazone)

- decrease insulin resistance
- worsen CHF
- linked to bladder cancer
- side effect : hepatotoxicity
D- incretin mimetics (exenatide, liraglutide) (GIP, GLP)

- given injection
- increase insulin release
- slow gastric motility
E- Dipeptidyl peptidase IV (DPP-IV) (Sitagliptin, saxagliptin)

- Prevent metabolism of incretins GIP, GLP
- Increase insulin release & slow stomach emptying
- given oral
II- Insulin. there is old regimen & new regimen
Old regimen

17
0.5 UI/KG = 2/3 morning + 1/3 Evening
2/3 NPH 1/3 Regular 1/2NPH 1/2 regular
New regimen 0.5UI/KG
50% glargine 50 %Lispro, asprat before meals
New type2 pt
GLP-L Can't used Metformin
not controlled
sulfonylureas
not controlled
Add glitazone switch insulin
New type l pt > insulin

Class Generic Name Brand name Dose/Day
Sulfonylureas Glybride, glipizide, Micronase, Diabeta, Amaryl 1-2
glimepiride
Bigunides Metformin Glucophage 2-3
Thiazolidinediones Roseiglitazone, - 1
pioglitazone
Glucosidase Acarbose, miglitol Precose With every
inhibitors meal
Meglitinides Repaglinide, - -
nateglinide
DPP- IV inhibitors Sitgliptin, Januvia, Onglyza, Tradjenta -
saxagliptin,
linagliptin
Subcutaneous agents
GLP-1 Exenatide, liraglutide Byetta, Victoza 2/day,
1/day
Type Peak Action (hours) Duration of Action (hours)

Ultra-Short-acting
1) Insluin lispro 30-60 min 4-6
2) Insluin aspart 20-30 min 3-5
Rapid
1) Regular 2-4 6-8
2) Semilente 2-6 10-12
Intermediate
1) NPH 6-12 12-18
2) Lente 6-12 12-18
Long- acting
1) Glargine 2 24
2) Levemir 18-24 36

18
Complications of Diabetes mellitus.
1- Acute complications:
I- Diabetic ketoacidosis (DKA).
Etiology: severe insulin insufficiency (type 1 DM)
Precipitating Factors:
1- interrupted insulin therapy 2- infection

3- emotional stress 4- excessive alcohol ingestion.
Clinical pictures:
1- Anorexia, nausea, vomiting abdominal pain

2- rapid breathing (kussmaul respiration), fruity breath odor of acetone.
3- Dehydration (dry skin, mucous membrane, poor skin turgor)
4- Altered consciousness to coma
5- Acidosis result fatal rhythm disturbance
Diagnosis:
1- high blood glucose.

2- High actoacetate, acetone, hydroxybutyrate
3- acidosis with high anion gap.
4- hyperK: but total levels of K depleted because urinary loss of K
Treatment:
1- normal saline
2- insulin Replacement (Bolus 5- 10 units of regular insulin)
3- Begin management wit IV insulin then switch to subcutaneous insulin
4- Overlap IV insulin and subcutaneous insulin for 6 -8 hour
5- Add 5% dextrose to normal saline when blood glucose 200-250 mg /dl an continue
IV insulin
6- K+ replecament
7- IV antibiotics + heparin ( for thrombosis )
8- HCO3 if PH < 7.0
II- hyperosmolar nonketotic coma (HONK)
Etiology: Type 2 diabetes
Precipitating Factor:
1- non compliance with treatment plus dehydration

19
2- Infection 3- strokes 4- steroids 5- immunosuppressant 6- diuretics
Clinical findings:
1- Weakness 2- ployuria 3- ploydipsia 4- lethargy 4- confusion 6- convulsions
7- coma
Diagnosis: lipid target in diabetics patient:
1- high blood glucose ≥ 700mg/DL 1- LDL <100 mg/dL (or <70 mg/dL in cases
of overt CVD)
2- High serum osmolaity
2- HDL >50 mg/dL
3- high BUN 3- Fasting triglycerides <150 mg/dL
4- acidosis 4- If LDL >100 mg/dl, patient should
5- no ketosis implement lifestyle modification (diet,
exercise) along with drug therapy : statin,
Treatment: fibrate or niacin but monitor patients
1- high volume fluid. closely for possible adverse reaction to
2- electrolyte Replacement therapy.
3- Insulin 5- Coronary artery bypass should be
performed in a diabetic patient even if
Chronic complications there is only 2-vessel coronary disease.
I- Cardiovascular complications. Note : The most common dyslipidemia in

patients with type 2 diabetes : high
number one cause of Death in triglyceride and low HDL cholesterol.
patients
II- Renal complication

− screening for proteinuria occur annually
− proteinuria > 300 𝑚𝑔 𝑝𝑟𝑜𝑡𝑖𝑒𝑛 /24 in urine
− -Microalbuminuria: 30-300mg protien /24 hour in urine
− Treated with ACEI, ARB
III- Eye complications:
− screening of retinopathy in type 2: annually once diagnosed

− screening of retinopathy in type 1: after 5 years of diagnosis
then annually
− proliferative retinopathy: vitreous hemorrhages or
neovascularization treated with laser photocoagulation
− nonproliferative retinopathy prevented by tight of glucose
levels
IV- Gastroparesis: metoclopramide or erythromycin
V- Erectile dysfunction: after 10 years of diabetes treatment: sildenafil

VI- Foot Exam: podiatric examination should annually

20
VII - Neuropath
1- peripheral neuropathy (most common): numbness, parasthesia, pain, absent

reflexes, loss of vibratory
2- Mononeuropathy: foot drop, wrist drop, paralysis of 3, 4, 6 cranial nerve
3- Autonomic neuropathy: orthostatic hypotension syncope, difficulty swallowing,
delayed gastric emptying, constipation, diarrhea, bladder dysfunction or paralysis,
impotence
Management: analgesics, gabapentin,pregabalin, amitriptyline, carbamazepine
VIII- Additional concepts
I- honeymoon period: symptom free interval after episode of DKA because stress
induced epinephrine release blocks insulin secretion
II- somogyi effect: hypoglycemia in middle night >> rebound hyperglycemia in

morning.
III- Dawn phenomenon: counter- regulatory hormones (cortisol, GH, epinephrine) >
hyperglycemia in morning
Hypoglycemia
Clinical pictures:
1- Secretion of epinephrine: sweating, tremor, tachycardia, anxiety, hunger

2- hypoglycemia: dizziness, headache, clouding vision- blunted mental activity loss
of Fine motor skills, convulsions, loss of consciousness.
classification:
1- postprandial y hypoglycemia
- After gastrectomy: gastrojejunostomy.
- due to hyperinsulinism
2- fasting hypoglycemia
etiology: hormone deficiencies (panhypopituitarism,adrenal insufficiency),enzyme

defect,substrate deficiency (malnutrition), liver disease, drugs

21
- hyperinsulinism: insulinoma, exogenous insulin, sulfonylureas, drugs, insulin

receptor antibodies
# Insulinoma: pancreatic B-cell tumor >> single and benign
Clinical pictures:blurred vision, headache, feeling detachment slurred speech,

weakness in early morning, late afternoon, after fasting
diagnosis: high insulin level 2- low glucose level < 40 mg /dl 3- CT scan, U/S,
arteriography to detect tumor
Treatment: surgery, diet, medical therapy
3- Factitious hyperinsulinism
Etiology: self- administrating of insulin or equal oral sulfonylureas
- Most often in health professions or access to these drugs
Diagnosis: triad of:
1- hypoglycemia 2- high immunoreactivity to insulin 3- plasma c- peptide
4- Ethanol: induced hypoglycemia.

22
ADRENAL GLAND
Cushing syndrome
- prolonged exposure to increase amount of cortisol or related corticosteroids.
Etiology:
1- exogenous: prolonged use of

glucocorticoids
2- adrenal hyperplasia:
- pituitary ACTH adenomas (most
common cause )
- nonendocrine tumor produce
ACTH OR CRH
(bronchogenic Ca, CA of thymus,
pancreatic CA)
3- Adrenal neoplasia
4- unknown source
Clinical picture: 1- fat deposition: moon face, buffalo hump, mesenteric bed, truncal
obesity 2- HTN 3- muscle weakness + fatigability 4- osteoporosis 5- cutaneous
striae 6- easy bruisability 7- acne, hirsutism, amenorrhea 8- emotional changes
irritability >> depression >> confusion 9- glucose intolerance >> DM 10-
hypokalemia 11 leukocytosis 12 delayed wound healing 13- Renal calculi 14-
glaucoma 15- pyuria 16- susceptibility to infection.
Diagnosis: 1- 1mg overnight dexamethasone suppression test (initial) 2- 24 hour

urine free cortisol (accurate) 3- midnight salivary cortisol 4- ACTH level 5-
high dose dexamethasone suppression test 6- CT, MRI 7- Sampling petrosal sinus.

23
Management:
1- surgical 2- medical: ketoconazole or metyrapone

24
Hyperaldosteronism
- function of aldosterone: 1- reabsorb NA+ + h2o 2- excrete k, H+
1- Primery aldosteronsim:
1- adrenal adenoma ( most common cause ) 2- Bilateral hyperplasia 3- licorice
2- secondary aldosteronism: dehydration, hemorrhage

25
Clinical pictures:
1- HTN
2- Muscle weakness, polyuria, polydipsia (low K)
3- Metabolic alkalosis.
Diagnosis:
1- Plasma aldosterone concentration

2- plasma renin activity: low in primary … high in secondary
3- NACL challenge test
Management:
1- adenoma removed surgically

2- bilateral hyperplasia: spironolactonec
-Bartter syndrome :defect in loop of Henle (defect of Na-K-2Cl cotransporter)
- loss of NaCl
- Hypotension, hypok, alkalosis
- -high renin + aldosterone
Congenital adrenal hyperplasia
Etiology: autosomal recessive with enzymes deficiency
C-21 hydroxylase deficiency: (most common)
- aldosterone deficiency: HypoNa, hyperk, dehydration, hypotension
- Female: ambiguous external genitalia, (enlarged) clitoris, partial or complete fusion

of labia … postnatally >> virilization
- Male: macrogentosomia …. postnatally > precocious puberty

26
2- C-11 Hydroxylase deficiency: (2 phase)
A. Early infancy: low aldosterone: hypotension, hyper k+

B. later in life: high aldosterone: hypertension, hypo k+
3- C-17 hydroxylase: hypogonadism, hypo k, hypertension
Diagnosis: serum testosterone, androstendine dehydroepiandrosterone, 17

hydroxyprogesterone, urinary 17- ketosteroid, pregnanetriol
Treatment: glucocorticoid Replacement
Adrenal insufficiency:
1- Primary insufficiency (addison disease)
2- secondary insufficiency:
Etiology:
1- idiopathic atrophy ( most common

cause)
2- autoimmune
3- surgical destruction,
4- hemorrhage,
5- trauma
6 - tumor
Clinical Pictures:
1- Weakness, paresthesias, cramping

2- intolerance to stress
C. personality changes
D. small heart, weight loss, sparse auxiliary hair.
E. hyperpigmentation of skin
27
F. hypotension
G. anorexia, weight loss, nausea, vomiting diarrhea, abdominal pain
Diagnosis:
1- neutropenia, lymphocytosis,
eosinophilia
2- hyperK, hypoNa
3- high Bun
4- low blood glucose
5- Low plasma cortisol
6- cosyntropin or ACTH
stimulation test (most accurate)
Differences between 2nd, 1st

insufficiency:
1- hyperpigmentation
2- electrolyte abnormalities
3- Hypotension
Treatment: glucocorticoid,
mineralocorticold, NaCl replacement, pt. education
Adrenal crisis
Etiology: 1- undiagnosed pt with adrenal insufficiency who has undergone surgery,

infection
2- Bilateral adrenal infarction or hemorrhage
3- sudden withdrawal chronic glucocorticoid therapy
Clinical Pictures: Fever, abdominal pain, vomiting altered mental status, collapse.
Treatment: 1- Cortisol, 2- IV fluids 3- hydrocortisone

28
Pheochromocytoma.
- Benign tumor arises from chromaffin cell of sympathetic nervous system.
Rule of 10%
- Familial pheochromcytoma, MEN IIA, IIB. Von recklinghausen neruofibromatosis,

von hippel lindau
Pathology:
- most common unilateral solitary lesion favor right side
- Extraadrenal: abdomen & near celiac, superior mesenteric, inferior mesenteric
ganglia.
Catecholamine secretion:
1- Dopamine: with familial syndrome & no HTN
2- Epinephine: causes tachycardia, sweating, flushing.
3- Norepinephrine: secrete from extraadrenal tumor
Clinical Pictures:
1- Attack of headache, sweating palpitations lasting from few minutes to several
hours
2- Chest or abdomen Pain
3- nausea + vomiting
4- HTN, anxiety, tremor, weight loss.
5- Death from cardiac arrhythmia + stroke
Diagnosis:
1- 24- hour urinary VMA, metanephrines. Free catecholamines (initial test)
2- clonidine- suppression test.
3- CT, MRI to localize tumor
4- MIBG (metaiodobenzylguanidine )
Treatment:
1- decrease Blood pressure with alpha Block Not with other medication.
2- surgical removal after stabilization.

29
DISEASES OF THE TESTES, HYPOGONADISM

- Primary hypogonadism: (High LH, FSH)
Klinefelter syndrome, anorchia, surgical or accidental castration, Infection (mumps)

chemotherapy.
- Secondary hypogonadism (Low LH, FSH)
- Hypopitutarism (Idiopathic, tumors)

- kallmann syndrome (hypogonadism & decrease sense of smell)
Clinical Findings:
I- Prepubertal: hypogonadism:
1- External genitalia underdeveloped. 2- high- pitched voice 3- bear doesn't grow
4- lack libido + potency
5- in adult: youthful appearance, obesity, disproportionated long extremities, small
Adam's apple 6- tests absent from scrotum
Diagnosis:
1- Low 17- ketosteroid.

2- Low serum testosterone
3- FSH, LH : low in hypothalamic or pituitary origin
high in primery testicular failure
Treatment: testosterone.
II- Postpubertal hypogonadism:
1- low libido, potency 2- retarded hair growth 3- vasomotor finding: flushing.

dizziness, chills. 4- lack of interest 5- sterility 6- muscle ache 7- back pain 8 -
skin is thin finely wrinkled.
Diagnosis: same prebubertal
Treatment: testosterone.

30
GYNECOMASTIA
Causes:
1- Physiological: growing infants, puberty

2- Cirrhosis of liver
3- Klinefelter's syndrome
4- Testicular cancer
5- Chronic renal failure
6- Hyperthyroidism
7- Drugs: spironolactone, CCB, ketoconazole, methyldopa, cimetidine, digoxin, drugs
of abuse (alcohol, heroin, marijuana)
METABOLIC SYNDROME
- Abdominal obesiy with 2 or more risk factor :
1- triacylglycerol >= 150 mg/dl
2- fasting blood glucose >= 100 mg / dl
3- blood pressure >= 130/85
4- HDL < 40 mg/dl men
< 50 mg/dl women
5- waist circumference >= 94 cm men
>= 80 cm women

31

32
Chapter 2
Rheumatology

33

34
Evaluating a patient with Arthritis
1. Number of joint
- Polyarticular: RA, SLE, parvovirus B19, HBV
- Monoarticular: gout, pseudogout, septic arthritis
2. Distribution of joint:
- Migratory arthropathy: rheumatic fever, Lyme disease, disseminated Gonococcal
infection.
- Oligoarticular: AS, osteoarthritis
3. Acute or chronic
- Acute: septic arthritis, gout
- Chronic: osteoarthritis
4. Systemic symptoms:
- SLE: pleural effusions, renal failure, psychosis, stroke.
- SJogren: dry eye/ mouth, parotid enlargement
- Systemic sclerosis. Skin involvement, Raynaud phenomena
- Osteoarthritis: no systemic symptoms.
5. Joint inflammations:
- Joint stiffness > 1 hour in morning
- Joint erythema, warmth
- ESR, CRP

35
TESTS IN RHEUMATOLOGIC DISEASES
1) Joint Aspiration (3Cs+ gram stain = cell count, crystals, culture)
Note:
- Septet arthritis < 50.000 WBC/ mm3 if antibiotics given before aspiration
- Culture of joint fluid is positive in only 50% or less of Gonococcal arthritis
2) Antinuclear antibodies:
- Antibodies binding to certain structures within the nucleus of cell
- Found in autoimmune disease

36
3) Rheumatoid factor:
- Autoantibody against the Fc portion of Ig G
- Neither sensitive nor specific for RA
- RF has prognostic significance
4) Antineutrophil cytoplasmic Ab
- CANA >> Wegener
- PANCA >> PAN, churg -strauss
RHEUMATOID ARTHRITIS
- Chronic inflammatory multisystemic disease with main target the synovium
Etiology: unknown
Risk factor:
1. Infections: mycoplasma,
parvovirus
2. Environmental factor: smoking
3. Women.
4. Age: 35-50 year
Pathogenesis:
1. Initiation phase:nonspecific
inflammation
2. Amplification phase: T- cell activation
3. Final phase: chronic inflammation + tissue injury
Note: disease of T- lymphocyte (HIV) will improve preexisting RA
Clinical pictures: (Diagnostic criteria) 4 of the following:

1. Morning stiffness > 1 hour for 6 week.
2. Swelling of wrist, MCP, PIP for 6 week.
3. Swelling of 3 joint for 6 week
4. Symmetric joint swelling for 6 week.
5. RF positive or anti - CCD
6. CRP, ESR
Joint NEVER involved:

37
1) DIPS 2) lower back
7. Extraarticular manifestations:
1) Damage to ligaments and tendons
- Radial deviation of wrist + ulnar
deviation of digits.
- Boutonniere deformity
- Swan- neck deformity
2) Rheumatoid nodules:
- Focal vasculitis over stress area
(occiput, Achilles, olecranon)
- Flare with Methotrexate
3) Felty syndrome (RA+

splenomegaly+ neutropenia)
4) caplan syndrome (RA+
pneumoconiosis)
- laboratory Findings:
1. RF or anti-ccp (more specific)
2. Anemia
3. -ESR, CRP
4. X- Ray
5. -Synovial fluid analysis
Diagnosis: (clinically)

38
Treatment:
1. NSAID (Aspirin)
- Cox2 inhibitor has no GIT effect
- refecoxib, valdecoxib>> increase risk of MI
2. Glucocorticoids: (short course only).
3. DMARD
- Antimalarial: Hydroxychloroquine
- Gold
- Sulfasalazine
- Methotrexate: best initial DMARD
- TNF receptor inhibitor: (infliximab, Adalimumab, Etanercept): Treatment of TB is
required before use them
Complication:
Aggressive disease: (poor prognosis)

1. High titer of RF
2. Diffuse rheumatoid nodules
3. Early joint erosions
4. Late age onset
5. Certain subtypes of HLA – DR4
1) atlantoaxial subluxation
- Neurologic symptoms >> paraplegia, quadriplegia, Neck pain, radicular pain,
myelopathy
- Diagnosis: x- rays cervical spin ct, MRI >>should done before intubation.
2) Ruptured Baker cyst : Swollen painful Calf
SYSTEMIC LUPHS ERYTHEMATOUS
- Systemic disease in which tissues and multiple organ are damaged by pathogenic
auto antibodies and immune complexes
Etiology:
39
- Unknown: abnormal response between the susceptible host and environmental

factor.
- UV- B light cause flares
Clinical pictures (Diagnostic criteria = 4 of the following:

1. Malar rash
2. Discoid rash
3. Photosensitivity
4. arthritis
5. Serositis (pleuritis or
pericarditis)
6. Renal involvement : lupus
nephritis >> ESRD ( most
common cuase of death )
7. Neurologic disorder (seizures or psychosis)
8. Hematologic disorder (hemolytic anemia, Leukopenia, thrombocytopenia)
9. Immunologic disorder (anti- dis DNA, anti- SM other ANAS).
Notes:
1. Arthritis identical to RA except non – erosive
2. Malar rash and photosensitivity rash is diffuse maculopapular flare with UV-
B light heals without scarring of the skin.
3. Discoid Rash circular rash with raised rim with central atrophy heals with scar.
4. All pt with renal involvement must undergo renal biopsy before treatment
5. Libman-sacks endocarditis: non infections endocarditis is occasionally seen in
lupus patients.
Diagnosis:
1. ANA: sensitive
2. Low complement (C3, C4)
3. High DS- DNA antibodies : specific
Treatment:
1. NSAID
2. Corticosteroids: cream, oral.
3. Antimalaria (Hydroxychloroquine)
4. Cytotoxic drugs ( azathioprine, cyclophosphamide)
5. Advised to wear protecting clothing sunglasses, sun block.
6. Belimumab inhibits B- cell activation.
Pregnancy and SLE

- Fertility is normal but abortions and stillbirth more common. Because anti-
phospholipid antibodies cause placental infarcts.
- Treated by low molecular high heparin in pregnancy

40
- All pregnant with lupus should screened for SSA/ anti- Ro antibodies which cross
placenta >> neonatal lupus +heart blocks.
DRUG- INDUCED LUPUS
- Hydralazine, isoniazid, procainamide, quinidine
Clinical picture.
- Fever, fatigue, arthritis, pleurisy
- No skin or kidney disease.
Diagnosis: anti- histone antibody sensitive
Treatment:
1. Stop medication
2. Symptoms resolve within 1-2 week. This confirms diagnosis
SCLERODERMA
- Chronic multisystem disease characterized clinically by thickening of skin caused by
accumulation of connection tissue +involvement of visceral organ
Clinical pictures:
1) GIT:
- esophageal dysmotility
- Hypomotility of small intestine
- Bacterial overgrowth and malabsorption
- Dilatation of large intestine
2) Lung:
- Pulmonary Fibrosis
- Restrictive lung disease
- Cor pulmonale
- Leading cause of death
3) Renal:
- Malignant HTN
- Acute renal failure

41
- Treated by ACE inhibitors

4) CREST syndrome (Limited scleroderma)
C= calcinosis= calcium deposits in soft tissue
R= Raynaud phenomenon
E= Esophageal dysfunction
S= sclerodactyly
T= Telangiectasias
- Skin involvement doesn’t extend above the elbow or above knee
Raynaud phenomenon
- Episodes of pallor or cyanosis in response to cold or emotional stimuli
- After rewarming the hands >> the blood flow will rebound and skin will appear
reddened.
Etiology: vasoconstriction of blood vessels that result in reduced blood flow, cyanosis
is created by deoxygenation of slow- flowing blood.
Clinical picture:
1. Sudden attack of pallor or cyanosis triggered by rapid changes in ambient

temperature.
2. Cold sensitivity of other area ear, nose, lower extremities.
Diagnosis:
1. Nailfold capillarscopy test: to differentiate between 1ry and 2nd Raynaud.
Treatment:
- Penicillamine
- CCB: nifedipine
- ACE inhibitor for HTN.

42
SJOGREN SYNDROME
Chronic autoimmune disease characterized by lymphocyte infiltration of the exocrine

glands.
clinical pictures :
- Itchy eyes, sandy Feeling >> keratoconjunctivitis

- Difficulty swallowing food.
- Parotid enlargement
Diagnosis:
- Schirmer test: decrease tear production

- Rose Bengal stain,corneal ulcerations
- ANA anti Ro 1 anti – La
- Biopsy of salivary glands = lymphocytic infiltrate
Treatment: no cure but symptomatic
- Pilocarpine and cevimeline increase Ach>> increase tear and saliva production.
SERONEGATIVE ARTHROPATHIES
SPONDYLOARTHROPTHIES
- Group of disorders share certain clinical features and association with HLA-B27

43
1) Ankylosing spondylitis
Etiology: unknown
- Affects axial skeleton and

peripheral joint
- Affect men 20-30 year
Clinical pictures:
- Chronic lower back pain

- Morning stiffness > 1 hour
improves with exercise
- Anterior uveitis
- Aortic insufficiency >> CHF, 3rd heart block
- on examination decrease spine mobility (schober test)
- Stress fractures
Diagnosis:
1. X- Ray: sacroiliitis, fusing of sacroiliac joint, bamboo spine of vertebral bodies.

2. HLA-B27, not used for diagnosis
Treatment:
- NSAID,physical Therapy exercise
- TNF blockers first than Methotrexate
2) Reactive Arthritis: 2 types

1) Reiter syndrome type 1:
-after non - Gonococcal urethritis (Chlamydia, ureaplasma

44
Clinical picture: keratoderma

blennorrhagica,circinate balanitis, oral or
genital ulcers, conjunctivitis and arthritis.
1) Reiter syndrome type 2:

- After diarrhea (campylobacter, Shigella ,
salmonella)
- Diagnosis: x- ray finding consistent with
seronegative spondyloarthropathy
Treatment:
1- Same as AS
2- tetracycline 3 week
3) Psoriatic arthritis
- involve DIP
- Psoriatic nail disease
- Sausage – shaped digit
- Peripheral arthritis
4) Enteropathic arthropathy
- Arthritis with IBD (UC, crohn)
- Pyoderma gangrenosum, erythema nodosum
HLA associated diseases:
- HLA B27 : seronegative arthiritis

- HLA DR 1,4,5,8 : rheumatoid arthritis
- HLA DR 3 : sjogren syndrome , SLE , celiac disease , type 1 DM (
also HLA DR 4) , graves disease , chronic active hepatit is

45
OSTEOARTHRITIS
- Destruction of articular cartilage with secondary remodeling and Hypertrophy of the
bone
- Not inflammatory disease
Risk factor
- Age -female sex - genetic factor - major joint trauma

repetitive stress -obesity
Eliology:
1. Idiopathic most common

2. Arthropathies (gout)
3. Endocrine disease (DM, acromegaly)
4. Deposition disease (hemochromatosis)
5. Mechanical factor (valgus / varus deformity)
- Most common joint: knee
Clinical pictures:
1) Joint pain increase with exercise relieved by rest

2) morning stiffness always < 20-30 min
3) Crepitation with joint movement
4) no systemic manifestations
Diagnosis: x ray: osteophytes and unequal joint space
- PIP = Bouchard's nodes

- DIP= Heberden’s nodes
Treatment:
1. Non pharmacological:
- Correction of poor posture
- Physical therapy
- Exercise program
- Weight loss
2. Pharmacological:
- Acetaminophen (4.000 mg/d)
- Ibuprofen (2.400 mg/d)
3. Capsaicin cream
4. Syx:joint arthroplasty
5. Intraarticular injection of hyaluronic

acid
46
CRYSTAL-INDUCED ARTHROPATHIS
Crystal deposit in joint:
- monosodium urate - Calcium oxalate -Calcium Pyrophosphate

- calcium hydroxyapatite
Gout:
- Deposition of urate crystals
Clinical pictures:
1) Podagra: red, warm, tender metatarsophalangeal joint of first toe.

2) Joint pain waking patient from sleep effect knee, ankle, PIP,DIP
Precipitating factor:
1- Excessive alcohol ingestions

2- Red meat intake
3- Trauma, surgery infections
4- Steroid withdrawal
5- Drug: diuretics, anti – TB
Diagnosis:
- Acute attack: analysis synovial fluid >>negative birefringent, needle shape crystal +
WBcs 5.000 – 50.000
- Chronic: Uric acid serum level
Treatment:
Acute:
1- NSAID
2- Steroid who can't tolerate NSAID
3- Colchicine : no effect on uric acid level

47
Chronic: (decrease Uric acid level)
1- Life style modifications: low purine diet, limitation of alcohol, avoiding diuretics.
2- Drug:
- Allopurinal : used in overproducer , undersecretor , renal failure
- Febuxostate : used in pt intolerant for allopurinal
- Pegloticase : used in refractory disease
- Probenecid : used in undersecretor
acute ‫ هجمات‬3 ‫ بعد أول هجمة بل بعد‬chronic ‫ال يجب معالجة المريض بال‬
Pseudogout:
- Calcium pyrophosphate crystal deposition
Risk factor 4Hs: Hyperparathyroidism,

hemochromatosis,Hypophosphatemia,Hypomagnesae
mia
Clinical picture: same as gout
Most common joint is knee
Diagnosis:
1- Synovial fluid analysis: rectangular, rhomboid

positive birefringent crystals
2- X- ray linear radiodense deposit in joint
menisci Or articular cartilage (chondrocalcinosis)
Treatment: same as gout
Prevent recurring with low doses colchicine

48
Temporal arteritis: (giant cell arteritis)
- Vasculitis affecting large arteries that supply head, eyes, optic nerves.
- Key: new onset headache in >50
age
- If not treated >> permanent vision
loss
Clinical pictures:
- Headache and pain in one or both temples.
- Scalp tenderness, pain on combing hair
- Jaw claudication (when chewing)
- Decrease vision
- Tongue numbness
- Neck stiffness due to polymyalgia
rheumatica
Diagnosis:
1. ESR initial test
2. Temporal artery biopsy
Treatment: corticosteroids start immediately if ESR elevated
-don’t withhold treatment to biopsy to be done.

49
INFLAMMATORY MYOPATHIES
- Inflammatory muscle disease: present with progressive muscle weakness include:

1. Polymyositis
2. Dermatomyositis
3. Inclusion body myositis
Clinical picture:
1- Proximal muscle weakness >> difficulty

in lifting objects, combing hair, getting up
from chair.
2- Distal muscle affected only in late stage.
3- Ocular muscles never affected (this
different than MG).
4- Dermatomyositis involve skin:
- Heliotrope rash>> purple lilac
discoloration of face, eyelid.
- Gottron’s papules are scaly lesion on knuckles
Diagnosis:
1- High CPK aldolase

2- Auto antibodies (anti – jo – 1)
3- Electromyography >> short duration, low
amplitude
4- Muscle biopsy >>confirmed
Treatment :
1- Steroid >>Polymyositis, Dermatomyositis

2- Immunosuppressive therapy >> inclusion body

50
Muscles
Disease CPK Pain Treatment Muscle biopsy Antibodies
affected
Proximal CD8 cell Anti jo1, anti
Polymyositis High painless cortison SRR (bad
muscles infiltrate
prognosis )
Anti M12
Dermatomyositis Proximal Cortisone or CD4, B cell (good
High Painless
muscles antimalarial infiltrate prognosis
51
Vacuoles and

Inclusion body Not responding No
Slightly high Painless Distal muscles inclusion
to cortisone autoantibody
bodies
Cortison Proximal
Normal Painless Stop cortison
muscles
statin Proximal
high Painful Stop statin
muscles
Erythema Nodosum
- Localized inflammatory condition of skin or panniculitis.
Etiology:
1. Streptococcal infection, coccidioidomycoses, histoplasmosis, enteric infection

Yersinia
2. Sarcoidosis, IBD
3. Syphilis, TB, hepatitis
4. Pregnancy
5. Medication: OCP, Sulfonamides
Clinical picture:
- Multiple, painful red, raised nodules on anterior surface of lower extremities

- Don’t ulcerate
- Last 6 week
Diagnosis:
ASLO if had recent r strept infection
Treatment:
- Analgesia, NSAID
-Potassium iodide Solution
Causes of high ESR :

1- chronic infection ( bacterial )
2- inflammation
3- anemia
4- malignancy
Causes of low ESR :

1- polycythemia
2- sickle cell anemia

52
Chapter 3
Gastroenterology

53

54
DISEASES OF THE ESOPHAGUS

1) Achalasia
Etiology: idiopathic loss of normal

neural structure of lower
esophageal sphincter
Clinical pictures:
- Dysphagia to both solids and

liquid simultaneous
- Regurgitation after eating>>
weight loss
- No relationship with alcohol or
tobacco use.
Diagnosis:
1. Esophagogastroduodenoscopay for alarm symptoms

1) Age >60 2) anemia 3) heme- positive stool 4) >6 month duration of
symptoms 5) weight loss.
2. X- ray:air fluid level

3. Barium: birds peak sign
4. Esophageal manometry: most accurate.
Treatment:
1) Pneumatic dilation (risk of perforation)
2) Botulinum toxin injections (needs reinjection)
3) Surgical myotomy (risk of reflux)
2) Esophageal cancer
1) Squamous cell cancer: proximal 2/3 of

esophagus
2) Adenocarcinoma: distal 1/3 of esophagus
Risk factor:
1) Squamous cell cancer: alcohol, tobacco use
2) Adenocarcinoma: GERD, Barrett esophagus
Clinical pictures:
1. Dysphagia: for solid then liquids.
2. Sever weight loss
3. Halitosis
55
4. Regurgitation
5. Hoarseness of voice
6. HyperCa
Diagnosis:
1. Barium swallow: initial test
2. CT detects of local spreads.
3. Endoscopy for biopsy
Treatment:
1. Surgical resection: Localized cancer
2. Chemotherapy (5-fu) + radiation: local meds.
3) Scleroderma (progressive systemic sclerosis)

Pathogenesis: atrophy and fibrosis of esophageal smooth muscle >> diminish
esophageal peristalsis
Clinical picture:
1. Dysphagia
2. GERD
3. History of scleroderma
Diagnosis: motility studies: most accurate
Treatment:
1. PPI
2. Metoclopramide
4) Diffuse esophageal spasm and

nutcracker Esophagus
Pathogenesis: idiopathic abnormalities of
neural process of the esophagus
Clinical pictures:
1. Intermittent chest pain simulate MI
2. Dysphagia
3. No relationship of exertion, or eating
4. Pain precipitated by cold liquids.
Diagnosis:
1. Barium studies : corkscrew sign
2. Manometric studies differentiate between the two diseases.
Treatment:
56
1. CCB: nifedipine 2.nitrates
5) Rings and webs:

Pathogenesis: thin epithelial membranes made out of squamous epithelial cells
-ring more distal at squamocolumnar junction.
- Plummer – Vinson syndrome more proximal at hypopharynx >> associated with
Iron deficiency anemia and squamous cell cancer.
Diagnosis: barium swallow
Treatment:
1. Dilation procedures
2. Plummer Vinson syndrome: treatment of iron deficiency anemia
6) Esophagitis:
Etiology
1. Infection: Candida albicans,HSV, CMV, aphthous
2. Inflammation medications (Fe- sulfate, alendronate, quinine, risedronate, vit-C,
KCL, NSAID, doxycycline.
Clinical pictures:
1. Odynophagia: painful swallowing
Diagnosis and treatment:

1. If Pt HIV: diagnosis confirmed by response to empiric treatment with
fluconazole. If doesn’t work then endoscopy should be performed
2. If inflammation from pills, advice pt to drink enough
water.
7) Zenker Diverticulum
Pathogenesis: out pocketing of posterior pharyngeal

constrictor muscles at the back of pharynx.
Clinical picture:
57
1. Bad breath smell

2. Difficulty of initiating swallowing
3. Clear throat and walking up with undigested regurgitated food on their pillow.
Diagnosis: barium studies:
Treatment:
- No endoscopy or NG tube.
- Surgical resection
8) Mallory Weiss syndrome
Pathogenesis: nontransmural tear of lower esophagus due to repeated retching and

vomiting.
Clinical picture:
Boerhaave syndrome:
1. Painless upper GIT bleeding
- Fu l l th ick n e s s tear s se co n d ary to
2. Black stool of bleeding > 100 ml ex trem e v o m it in g
3. Hematemesis - Co m m o n in a lco h o li cs
4. No dysphagia or odynophagia - Mo s t co m m o n lo cat io n : left p o s tero la tral
asp e ct o f d i st al eso p h ag u s
- Diag n o s is : g a s tro g raf in eso p h ag ram
Diagnosis: upper endoscopy
- Treat m en t : su rg i ca l ex p l o ratio n w ith
d eb rid em en t o f m ed ia st i n u m an d c lo su re
Treatment: o f th e wo u n d
1. Resolve spontaneously No te : m o st co m m o n cau se o f
2. Injection of tear with epinephrine eso p h ag ea l p erfo r at io n i s i atro g en ic
(u p p er e n d o sco p y
3. Cauterization

58
EPIGASTRIC PAIN
Etiology:
1- Gastroesophageal reflux disease 2-Ulcer disease
3- Gastritis 4- pancreatitis 5- gastric cancer
6- Nonulcer dyspepsia
Note: - most common cause of epigastric tenderness >> pancreatitis

- Most common cause of epigastric pain >> nonulcer dyspepsia
Gastroesophageal Reflux Disease:
Etiology: abnormal flow of the acid gastric contents backward from the stomach up
into the esophagus
Risk factor: nicotine, alcohol, caffeine, peppermint, chocolate anticholincrgics,

calcium-channel blocker, nitrates
Clinical Pictures:
1-Dyspepsia or epigastric pain 2-sore throat 3-cough and wheezing 4- bad metal-
like taste in the mouth 5- hoarseness 6- pain in the substernal area.
Diagnosis:
1- Clinical presentation
2- 24-hour pH monitor: The most accurate diagnostic test
Treatment:
1- Modify their lifestyle: avoiding nicotine, alcohol, caffeine, hocolate, and late-night
meals, elevating the head of the bed 6 to 8 inches with blocks
2- PPIs: Omeprazole, esomeprazole, lansoprazole, pantoprazole
3- Nissen fundoplication
4- Circular purse-string suture
5- H2 blockers for very mild,
intermittent symptoms.
6- Prokinetic drugs: such as
metociopramide

59
Barrett Esophagus
Etiology:
Long-standing reflux disease the epithelium of the lower esophagus undergoes
histologic change from a normal squamous epithelium to a columnar epithelium.
Diagnosis:
Barrett esophagus >> endoscopy every 2 - 3 years
Low grade dysplasia >> endoscopy in 3 to 6 months
High grade dysplasia >> distal esophagectomy or an endoscopic mucosal resection
Treatment: PPIs
Peptic Ulcer Disease

Etiology:
1- NSAIDs 2-Helicobacter pylori infection 3-stomach cancer
4- Zollinger-Ellison syndrome 5-Crohn disease 6-burns 7-head
trauma 8- prolonged intubation and mechanical ventilation
Notes:
- NSAIDs decrease the normal production of the mucous
barrier
- Stress ulcers from burns and head trauma result from an intense vasoconstriction
of the vasculature that supplies the gastric mucosa
Stomach distention amino acid vagus
Histamine Gastrin acetylcholine
ACID
somat osta ti n
secretin

60
- Most important stimulant to gastrin release is distention of the stomach.

- The most common cause of ulcer disease is Helicobacter
pylori
Clinical pictures:
1- Gastric ulcer >>pain on eating
2- duodenal >> pain relieved by eating
3- Nausea and vomiting
Diagnosis:
1- Upper endoscopy.
2- Barium studies
3- The diagnosis of H. pylori :
a- Serology: least expensive, least invasive,
high sensitivity
b- urea breath testing have the same sensitivity as serology and

are able to easily disti nguish new versus
c- stool antigen testing old disease.
d- biopsy with histology :most sensitive and specific test known as CLO test
Treatment:
‫منبلش‬PPI +clarithromycin +amoxicillin 14 days
‫منعمل‬urea breath test
‫اذا البكتريا لسا موجوده‬
‫منعطي‬tetracycline + metronidazole + bismuth subsalicylate 14 day
‫اذا البكتريا راحت ولسا القرحه موجوده‬
Zolliner –Ellsion syndrome

61
Indications for surgery in PUD:

• UGI bleeding not amenable to endoscopic procedures
• Perforation
• Refractory ulcers
• Gastric outlet obstruction
Gastritis:
Etiology: inflammation, erosion, or damage of the gastric lining by NSAIDs,

Helicobacter, head trauma, burns mechanical ventilations
Types:
1- Type A >> atrophy of the gastric mucosa and is associated with autoimmune
processes + achlorhydria
2- Type B >>most common type of gastritis. It is also associated with increased
gastric acid production.
Clinical picture:
1- symptomatic bleeding 2- abdominal pain 3-Nausea +
vomiting 4- hematemesis or melena
Diagnosis: low vitamin BI2 level
Treatment: vitamin BI2 replacement
Zollinger-Ellison Syndrome
Etiology: cancer of the gastrin-producing cells for unknown cause
- 50 % in the duodenum, 25 % in the pancreas. A small percentage MEN1
Clinical pictures:
1- Ulcers >> recurrent after therapy, multiple in number, and occur in the distal
portion of the duodenum or resistant to routine therapy.
2- Diarrhea
3- Steatorrhea because lipase inactivated by acid
Diagnosis
1- elevated gastrin > Other causes of high gastrin are:

• Pernicious anemia
• Chronic gastritis
• Renal failure
• Hyperthyroidism

62
2- Secretin test
3- CT, MRI, US nuclear test, somatostatin-receptor scintigraphy, endoscopic
ultrasound to Localize the disease.
Treatment: localized disease >> surgically resected

Metastatic disease >> long-term administration of PPls
Gastroparesis: (weak stomach)
Etiology:
- Diabetes
- Electrolyte problems (potassium, magnesium, calcium (
Clinical pictures:
- early satiety - postprandial nausea -increased abdominal fullness
(This is from decreased motility of the stomach and the accumulation of food there)
Diagnosis :gastric-emptying study
Treatment: erythromycin or metoclopramide
Dumping Syndrome
Etiology: vagotomy and gastric resection were performed to treat severe ulcer disease.
Clinical pictures: sweating, shaking, palpitations, and lightheadedness shortly after a

meal.
Treatment: eat multiple small meals
Nonulcer Dyspepsia
- When all the causes of epigastric pain have been excluded>> nonulcer dyspepsia
- The cause of nonulcer dyspepsia is unknown.

63
INFLAMMATORY BOWEL DISEASE
- idiopathic disorders of the bowel

Crohns IBD Ulcerative colitis
C/P mouth to anus Diarrhea large intestine

Transmural Bleeding mucosa
Mass Wight loss ulcer
Fistula formation Abdominal pain no fistula
Skip lesion Barium colon

String sign
DX
Low ANCA Antibodies high ANCA

High ASCA low ASCA
Endoscopy
Malabsorption episcleritis
Vit b12 Scleritis
comp
vit K >> high pt iritis
Irion >anemia Sclerosing cholangitis
Kidney stone skin (Pyoderma, erythema) fat
malabsorption>high oxalate colon cancer (8-10 years)
Tx Pentasa mesalamine ROWASA

ASACAL
cipro/metronidazole steroid for acute
pernial disease
azathiopruine syx
Infliximab 6 mercaptine

64
Diarrhea
Either an increased frequency or volume of stool per day
Etiology: infection, antibiotics associated, lactose intolerance, IBS, carcinoid
Treatment:
- If the patient is hypotensive, febrile, and having abdominal pain, >>admitted to

the hospital and given intravenous fluids and antibiotics.
- The presence of blood in the stool is especially serious and is probably the single
strongest indication for the use of antibiotics.
Infectious diarrhea
Diagnosis:
1- Stool for fecal leukocytes is the most useful test
- Diarrhea with WBCs / RBCs: salmonella, shigella, Yersinia, campylobacter,

E.coli, vibrio parahaemolytics, vibro vulnificus
2- Cryptosporidiosis,:a modified acid-fast
3- Giardia:ELISA stool antigen test
Treatment:
1- resolve spontaneously
2- antimicrobial therapy if there is abdominal pain, blood in the stool, and fever
Antibiotics (ciprofloxacin or the other fluoroquinolones ± metronidazole)
3- Scombroid poisoning: antihistamines, diphenhydramine.
4- Giardia: metronidazole or newer agent tinidazole
5- There is no specific therapy for viral diarrhea.

65
Antibiotic – Associated Diarrhea

- following use antibiotics
- benign self limited
- no pathogens are identified
- caused by changes in function and composition of intestinal flora + increase
motility (erythromycin)
- Treatment : supportive + discontinuation of antibiotics

66
C. difficile-Associated Diarrhea (pseudomembranous colitis)
Etiology:
- using antibiotics change intestinal flora lead to overgrowth C.difficile
- C.difficile produce toxins A and B which bind to intestinal receptors
most common antibiotics:

1- Clindamycin
2- Fluoroquinolones
3- Cephalosporins
Clinical pictures:
- Mild diarrhea to fulminant colitis after using antibiotics
Diagnosis:
1- ELISA: in the past
2- Nucleic acid amplification assay (LAMP, PCR): detect toxin A, B gene
Treatment:
- Oral Metronidazole: is the drug of choice
- IV metronidazole: Unable to use oral medication
- Oral vancomycin indication: not respond to metronidazole
Lactose Intolerance
Etiology: lactase deficiency
Clinical Pictures:
- Diarrhea NO has blood or leukocytes -gas and bloating
- NO weight loss.
Diagnosis:
- Increased stool osmolality and increased osmolar gap. The osmolar gap means
that the difference between the osmolality measure in the stool and the osmolality
calculated from the sodium and potassium
- routine way remove milk, cheese, ice cream, and all other dairy products
resolution of symptoms, within 24 hr
Treatment:
- dietary changes are the best therapy
- The patient can use lactase supplements.

67
Irritable Bowel Syndrome

Etiology: pain syndrome of unknown etiology
- increased frequency of the normal peristaltic and segmentation contractions of the
bowel
Clinical Pictures
- Constipation only
- OR diarrhea alone
- OR diarrhea alternating with constipation.
- Everyone has pain.
- NO nocturnal symptoms
- NO constitutional signs or symptoms, such as fever, weight loss, anorexia, or

anemia.
Diagnosis:
- no specific test
- diagnostic criteria, Rome criteria, must occur for at least 3 months:
1- Pain relieved by a bowel movement or by a change in bowel habit (e.g.,
when you develop diarrhea, the pain goes away)
2- Fewer symptoms at night
3- Diarrhea alternating with constipation
Treatment:
- There is no clear definitive therapy for IBS.
- All patients should be placed on a high fiber diet
- antidiarrheal agents, loperamide or diphenoxylate for diarrhea-predominant
disease
Antispasmodic agents:hyoscyamine, dicyclomine, and the belladonna alkaloids
- tricyclic antidepressants
- Newer agent: tegaserod, alosetron (work on serotonin levels in the bowel).
Carcinoid Syndrome
Etiology: tumors of the neuroendocrine system
Site: appendix, ileum, bronchus
Note: serotonin produced from a bronchial carcinoid does not get detoxified in the
liver and is released directly into the circulation
Clinical Pictures:
68
-Diarrhea -flushing -tachycardia -

hypotension - rash may develop from niacin
deficiency -Endocardial
fibrosis this leads to tricuspid insufficiency and
pulmonic stenosis.
Diagnosis:
Urinary 5-hydroxyindolacetic acid level
(5HIAA).
Treatment:
- Octreotide :somatostatin analog
- Surgical resection.
MALABSORPTION SYNDROMES
Etiology:
1- celiac disease
2- chronic pancreatitis
3- tropical sprue
4- Whipple disease
Clinical pictures:
- Steatorrhea:greasy, oily, floating, and fatty, with a particularly foul smell, as if fat
were fermenting
- weight loss : fat has the highest caloric
content of all the foods
- Malabsorption of fat-soluble vitamins
AKED >>hypocalcemia, easy bruising,
prolongation of the prothrombin time.
- Iron malabsorption from duodenum
- Folate malabsorption
- Vitamin Bl2 malabsorption from terminal
ileum.
- dermatitis herpetiformis vesicular skin rash on the extensor surfaces of the body
seen in celiac disease
- Chronic pancreatitis: repeated episodes of pancreatitis from alcohol or gallstones.
- Tropical sprue :a history of being in a tropical country
- Whipple disease: dementia, arthralgia, ophthalmoplegia.
Diagnosis:

69
1- For celiac disease:

- Antiendomysial and antitransglutaminase antigliadin antibodies.
- A small bowel biopsy, which shows flattening of villi. Most accurate test.
2- For Chronic pancreatitis

- history of repeated episodes of pancreatitis
- Calcification of the pancreas on x-ray and CT scan.
- a Secretin test: most accurate test
- D-xylose: to distinguish between celiac disease and chronic
pancreatitis.
3- For Tropical sprue: biopsy
4- Whipple's disease: biopsy, a polymerase chain reaction (PCR)
of the bowel biopsy. A positive Tropheryma Whippelii biopsy shows foamy
macrophages that are PAS positive.
Treatment:
- Celiac disease: a gluten-free diet (no wheat, oats, rye,or barley).
- Chronic pancreatitis: orally replacing all the deficient enzymes>>
Amylase, lipase, and trypsin
- Tropical sprue: trimethoprim/sulfamethoxazole or doxycycline for 6 months.
- Whipple's disease: trimethoprim/sulfamethoxazole or doxycycline
for 1 year.
DIVERTICULAR DISEASES
Diverticulosis:
Etiology: a lack of fiber in the diet to >> rise in intracolonic

pressure >> outpocketing of the colon
Clinical Pictures:
1- Asymptomatic
2- left lower quadrant abdominal pain that can be colicky
in nature.
3- bleeding occurs more often from diverticula on the
right because of thinner
4- Diverticula are more common on the left in the sigmoid
Diagnosis:
1- colonoscopy.
2- barium studies
Treatment:
70
- increasing fiber in the diet with products
Diverticulitis
Etiology :
infection occurring in one of the diverticula. Due to blockage of the diverticular
entrance from nuts or corn.
Clinical Pictures:
- fever -tenderness, pain - elevation WBCS
Diagnosis
- CT scanning.
- Barium studies and endoscopy are contraindicated
Treatment:
- ampicillin/sulbactam, piperacillin/tazobactam
CONSTIPATION
Etiology:
1- lack of dietary fiber and insufficient fluid intake (most common cause)
2- Calcium-channel blockers 3- oral ferrous sulfate
4- hypothyroidism 5-opiate
6- medications with anticholinergic effects: tricyclic antidepressants
Treatment:
- stop medications that cause constipation
- hydration.
- Bulking agents
- Drug treatment
- Enemas for acute constipation

71
COLON CANCER
Risk factor:
- high diet in red meat and fat ` -smoking
Clinical Pictures:
- right side colon >> -heme-positive, brown stool - chronic anemia
- Left side colon,cancer of the sigmoid >> symptoms of obstruction and with
narrowing of stool caliber
Diagnosis: Ty p es o f p o ly p :
1- Colonoscopy :most accurate
1- Hyperplastic: nonmalignant
2- Barium studies:less accurate
2- hamartomatous: nonmalignant
Treatment: 3- Inflammatory: nonmalignant
4- Adenoma:
- Localized cancer to the mucosa,
i. Villous: malignant.
submucosa, and muscularis layers can
ii. Tubulovillous: less
easily be resected and cured malignant
- Widespread disease >>chemotherapy iii. tubular: least malignant
5-fluorouracil
Screening:
1- Annual fecal occult blood testing
2- Colonoscopy every 10 years after age 50
- False positive: red meat, and poultry.
- False-negative :vitamin C.
Note:
- previous colonoscopy shows polyps >>repeat colonoscopy 3 - 5 years.
- In those who have a family history of colon cancer, screening should begin at age
40, or 10 years earlier than the family member, whichever is younger.
Hereditary Nonpolyposis Syndrome (Lynch Syndrome)

- There are certain families who carry a genetic defect with a high degree of colon
cancer.
- 3 family members in at least 2 generations with colon cancer. one of these cases
age <50.
- very high incidence of ovarian and endometrial cancer
Screening:start at age 25 and undergo colonoscopy every 1 - 2 years.

72
Hereditary Polyposis Syndromes:

- genetic defect with 100% for development of
adenomas by the age of 35 and colon cancer by
the age of 50.
Screening: Flexible sigmoidoscopy start at age 12
every 1 - 2 years
juvenile polyposis syndrome

- only a few dozen polyps, (thousands of polyps in familial polyposis syn)
- the polyps hamartomas, not adenomas.
Cowden syndrome
- hamartomas with slightly increased risk of
cancer
- present with rectal bleeding in a child.
Screening: There is no recommendation
Other Polyposis and Colon Cancer Syndrome

1- Gardner syndrome :colon cancer + multiple, soft-tissue tumors, such as
osteomas, lipomas, cysts, and fibrosarcomas.
2- Peutz-Jeghers syndrome: hamartomatous polyps + hyperpigmented spots. on the
lips, buccal mucosa, and skin. Most common
presentation is with abdominal pain due to intussusception/bowel obstruction
3- Turcot syndrome:colon cancer+ CNS malignancies
Screening. There is no recommendation
Note: endocarditis from Streptococcus bovis >> do colonoscopy

73
GASTROINTESTINAL BLEEDING
Etiology:
1- The most common causes of upper GIT bleeding:
- ulcer disease - gastritis - Mallory- Weiss syndrome,
- esophagitis - gastric cancer.
- Variceal bleeding is common from cirrhosis.
- aortoenteric fistula: history of abdominal aortic aneurysm repair
2- most common cause of lower GIT bleeding:
- diverticulosis - angiodysplasia (also known

as AVM or vascular ectasia)
- hemorrhoids - cancer. - IBD
Note: upper GIT bleeding: is bleeding occurring proximal to the ligament of Treitz,
which anatomically separates the duodenum from the jejunum.
Clinical presentation.
1- lower GIT bleeding: red blood in the stool,
2- upper GIT bleeding: black stool, melena, hematemesis
3- orthostasis
Diagnosis:
1- Endoscopy is the most accurate test
2- A nuclear bleeding scan can detect low volume bleeds
3- Angiography :higher volume of blood loss
4- capsule endoscopy
Treatment.
1- fluid resuscitation with normal saline or Ringer's lactate.
2- CBC >>
- Platelets transfused if the platelet count is <50,OOO/mm3
- The hematocrit should be maintained at 30% or above in older patients and
above 20 % in young patients

74
3- prothrombin time: if high give fresh

frozen plasma Indications of TIBS :
4- crossmatch and type and 1 - Refractory cirrhotic
5- Patients with gastritis or the possibility hydrothorax
2 - Refractory ascites
of ulcer disease should be treated with
3 - Recurrent vascular bleeding
PPIs
4 - Pt waiting for liver
6- Esophageal varices are treated with transplant
octreotide if fails >> do
bands if fails >> TIPS (transjugular
intrahepatic portosystemic shunting).
7- Propranolol used in portal hypertension
- More than 80% of gastrointestinal bleeding cases will stop spontaneously with
appropriate fluid resuscitation,
ACUTE PANCREATITIS
Etiology:
Most common alcoholism and gallstones
Clinical Presentation:
1- Midepigastric pain with tenderness radiates straight through to the back, a rigid
abdomen
2- Nausea, vomiting
3- fever, hypotension
4- respiratory distress from ARDS
5- Cullen sing, turners sign
6- Ascites, pleural effusion
7- Splenic vien thrombosis

75
Diagnosis.:
1- amylase and lipase level (The initial tests)>>
Lipase is more specific to the pancreas
2- hyperglycemia
3- Hypocalcemia
4- high BUN because of intravascular volume
depletion.
5- CT scan most accurate test
6- Ranson criteria.
7- ERCP The single most accurate test for the detection of biliary and pancreatic
ductal pathology
8- Urinary assay of trypsinogen activation peptide (TAP
Treatment.
- There is no specific therapy to reverse pancreatitis.
- supportive, with intravenous fluids, bowel rest, and pain medication.
- ERCP to remove a stone in the pancreatic duct or to dilate a stricture.
- Antibiotics(imipenem or meropenem) for pancreatitis is very severe(>30%
necrosis visible on the CT scan)
- percutaneous needle biopsy for Severe necrosis (persistent fever)
- surgical debridement for infection of the pancreas with necrosis
Notes:
1- pancreatitic abscess begin for 4 to 6 weeks after pancreatitis.
2- Pseudo cysts develop 2 to 4 weeks after pancreatitis >>should be
drained if there is: pain, fistula, rupture or expanding.

76
LIVER DISEASE AND CIRRHOSIS
- Cirrhosis develops when there is chronic and severe inflammation of the liver for
an extended period of time.
Etiology:
1- primary biliary cirrhosis, 2-sclerosing cholangitis,
3- alpha-1 antitrypsin deficiency, 4- hemochromatosis,
5- Wilson disease. 6- chronic hepatitis B and C
Clinical Pictures:
1- portal hypertension 2- esophageal varices, 3-ascites,

4- peripheral edema 5-spider angiomata, 5- palmar erythema, 6-asterixis,
encephalopathy 7- Jaundice
8-Spontaneous bacterial peritonitis (SBP):
- idiopathic infection of ascites.
- Gram stain is rarely positive.
- culture of the fluid is the most specific test, but we cannot wait so check WBCS
>5OO/mm3 or the presence of >250/mm3 >> start antibiotics (Cefotaxime or
ceftriaxone)
Serum-Ascites Albumin Gradient =the serum albumin - ascites albumin

- SAAG > 1.1, portal hypertension, as cirrhosis.
- SAAG <1.1 Cancer and infections
Treatment:
- no specific therapy just manages the complications:
1- ascites >>diuretics spironolactone.
2- Portal hypertension and varices >> Propranolol
3- Encephalopathy >> neomycin + lactulose

77
Primary Biliary Cirrhosis

Etiology: idiopathic autoimmune disease common in middle age female
Clinical pictures: fatigue and pruritus
Diagnosis:
1- Normal ALT, AST
2- High alkaline phosphatase +gamma glutamyl transpeptidase (GGTP)
3- High IgM
4- Antimitochondrial Ab specific test
5- Liver biopsy most specific
Treatment ;
1- Bile acid medication >> ursodeoxycholic acid and cholestyramine
2- UV light for pruritus
3- Liver transplant
Primary Sclerosis Cholangitis

Etiology: idiopathic disease of biliary system
- With IBD (more with UC )
Clinical pictures: same as primary biliary cirrhosis
Diagnosis: same as primary biliary cirrhosis EXCEPT:
1- Antimitochondrial test is negative
2- ERCP most specific
Treatment: same primary biliary cirrhosis
Hemochromatosis
Etiology: over absorption of iron in the duodenum
Clinical picture:
1- Liver cirrhosis and hepatocellular cancer
2- Restrictive cardiomyopathy 3- arthralgia 3-skin hyperpigmentation

78
4-DM 5-hypogonadism 6-vibro vulnificus and Yersinia infection
Diagnosis:
1- High iron land ferritin
2- Low TIBC
3- Liver biopsy and

C282Y gene: most accurate
Treatment:
1- Phlebotomy
2- Deferoxamine and
deferasirox
Wilson Disease
Etiology: AR disease with
decrease excretion and increase
absorption of copper
Clinical pictures:
1- Brian: abnormal movement, psychiatric
disturbance
2- Eye: kayser – Fleischer rings
3- Kidney: fanconi syndrome, tubular
acidosis type 2
Diagnosis:
1- Low ceruplasmin level
2- High urinary copper
3- Liver biopsy: most accurate
Treatment:
1- Copper chelators:Penicillamine, trientine
2- Oral zinc decrease copper absorption
3- Liver transplantation

79
Alpha -1 Antitrypsin Deficiency

Etiology: AR disease
Clinical pictures: cirrhosis + emphysema in young nonsmoker
Diagnosis: blood test for AATD:
1- Alpha-1 genotyping: determines genotype
2- AAT PI type of phenotype: determines the type of AAT protein
3- AAT level test: determines the amount of AAT in a person’s blood
Treatment: enzyme replacement + stop smoking
Chronic Hepatitis B and C

Etiology: virus transmitted by blood products, needlestick injury, sex
Clinical pictures: asymptomatic until advanced
Diagnosis:
- Chronic HBV: HBVs Ag > 6 month
- Chronic HCV: HCV Ab + high viral load by PCR
- Liver biopsy most accurate
Treatment:
- HBV: interferon / lamivudine / entecavir / telbivudine /adefovir
- HCV: interferon +ribavirin + telaprevir / boceprevir

80
Chapter 4
Cardiology

81
‫‪Chapter 4 : Cardiology‬‬
‫الدكتور يزن ابو غربيه ‪0795407665‬‬

‫‪82‬‬
Patient with acute chest pain

1- History:
1- Duration 2- Quality
3- Location 4- radiation
5- Frequency 6- alleviating Factor 7- Associated symptoms
Some headlines to remember

1- Stable angina & ACS chest Pain is (tightness, heaviness, pressure)
2- Inferoposterior wall Ischemia.
>> Nausea + Vomiting + bradycardia + Hypotension (Vagal reflex)
3- sharp or Knife- like chest pain > >muscle, skeletal disorder
4- MI Pain >> 20 - 30 minutes
5- Chest Pain responses to NTG. > MI
6- Chest pain not responses to NTG > GERD
7- Women + older people > atypical symptoms: Dyspnea + SOB
2- Physical Ex:
i- V/s: 1- Initial Impression:
Diaphoresis, Tachypnea, anxious >
aortic dissection
2- Pulse
3- Temperature: Fever > Pneumonia
4- Blood pressure
ii- Chest wall Auscultation:
Normally S1: Mitral >> tricuspid
S2: Aortic>> Plu
Wide splitting Paradoxical splitting

Aortic Plu Plu Aortic
1- R B B B. 1- L B B B
2- Plu/ HTN. 2- HTN
3- PS 3- AS
4- RVH 4- LVH
3- Testing
I- ECG. Most Important test
II- Cardiac Biomarker
1- CK- MB:
Appears 4-6 hour
Peak 12-24 hour
Normal 2-3days
Should be Repeated 6- 12 hour

83
CPK high in: MI, trauma, exercise,

myositis, afro-Caribbeans, hypothermia,
hypothyroidism
2- Troponin:
Appear 4-6 hour
Normal 2-3weeks
Should be repeated 6-12 hour
Troponin high in: MI,
HF,pneumonia, trauma, renal
failure, aortic valve disease, PE,
septic shock
3-Myoglobin: appear 1-4 hour (earliest): not specific
4-AST, LDH (latest): not specific
III- Chest x ray: pneumothorax, pleural effusion
IV-Other test ABG,BNP,CT scan Causes of chest pain

84
aortic dissection - sharp tearing pain radiate to back

-loss of pulse
-widened mediastinum X RAY
- diagnosis: MRI, CT
Pulmonary embolism -dyspnea, tachycardia

-Hypoxemia -chest pain pleuritic
-ECG S1 Q3 T3
-Diagnosis: spirial CT
myocarditis -vague chest pain after viral illness

- High CKMB
- ECG abnormal Q waves
Musculoskeletal disorder (costochondritis, Cervical osteoarthritis, radiculitis)

- Chest Pain stabbing, localized, pleuritic Increase with motion or palpitation
- ECG normal
GIT Disorder
1-GERD: after meal+ relieved by antacids
2- Diffuse esophageal spasm: after cold liquid relieved by NTG diagnosed by
endoscopy, esophageal manometer
3- Peptic ulcer, Pancreatitis, cholecystitis
Pneumothorax:
1_ abrupt sharp chest pain
2_ absent breath sound
3_ chest x-ray
Pleuritis: - Sharp pain increase after inspiration

- friction rub
- other respiratory symptom after infection

85
Ischemic heart disease
- It is imbalance in coronary oxygen demand & supply

- Most common cause: atherosclerosis.
Major Modifiable Riske factor

1- elevated cholesterol: 1-low HDL 2- high LDL 3-high TAG
4-high Total/HDL 5- high lipoprotein A
2- Tobacco
3- HTN
4- Decrease Physical activity exercise
5- Obesity
6- DM
Major Uncontrolled Risk Factor

1- Age ≥ 65 year
2- Sex: men greater Risk Factor
3- Heredity: Family history of premature disease (< 55 male …< 65 female)
Major Contributing Factor

1- Sex hormones
2- stress
Myocardial Ischemia as manifestation of IHD

- There is 2 types
1- Ischemia occurs due to Increase demand.
 demand ischemia (Stable angina)
2- Ischemia occurs due to cessation of blood
 supply Ischemia. (MI, Unstable Angina)
Stable Angina

86
- Etiology: Atherosclerosis reduce Blood supply
- Clinical Pictures:
1- substernal Pressure lasting 5-15 minutes
2- Radiate to Jaw, neck, shoulder, and arm
3- Increase on exertion (exercise)
4-Atypical symptoms: weakness, breathlessness with elderly, DM
5-Physical Exam: s4 heard
- Diagnosis: If ECG done during attack, it will show ST - depression) ‫يعني المريض‬
‫)إذا إجا على الطوارئ وهو عنده النوبة‬
‫الفحوصات اآلتية تطلب عندما يأتي المريض إلى عيادة القلب‬

1- Baseline ECG: to see If there is previous MI or arrhythmias
2- Exercise stress test:
- Positive If there is
-ST depression > 2 mm
-Hypotension > 10 𝑚𝑚 𝐻𝑦
- Uses of stress test

1- Determine severity of IHD ‫مرضو اسوء‬
‫المريض اللي بتعب أسرع‬
2- Assessing the effect of treatment
3- After MI to determine functional
capacity
Contraindication:
1- aortic dissection
2- Acute MI
3- Unstable angina
4- Sever CHF
5- Uncontrolled ventricular
arrhythmias
6- Aortic stenosis
7- Hypertrophic cardiomyopathy
8- Uncontrolled hypertension
Some drug affects the ECG:

1- BB: decrease Heart Rate
2- BB, NTG, alpha blocker: cause
hypotension
3- Digoxin: depress ST Segments

87
- Other test
1-Nuclear stress test: IF there is changing in baseline ECG
2- Dobutamine / adenosine. Stress rest: Patient who are unable to exercise.
3-Stress Echo: To recognize abnormal movement of walls heart
4- Invasive techniques: cardiac catheterization
- Treatment
A- Medical:
1- NTG: LONG + Short acting (3min)
2- BB: LONG
3- Aspirin
4- Lipid lowering (statins)
Lipid lowering treatment:

Target goal:
1- LDL < 100 mg/dl
2- HDL >= 40 mg /dl
3- TAG < 150 mg/dl
Side effect of statin:

1-myalgia: most common
2-abdomen discomfort
3-high ALT, AST (hepatitis)
4-CPK (myositis)
5-Rhabdomyolysis : most
dangerous
B- Coronary bypass graft (CABG): if there is

. 3 vessels + LV dysfunction + low EF
. Left main coronary disease
. Fail medical therapy or side effect
C- Precautious coronary intervention (PCI): if there is

- Stent now the standard
- 1-2 vessels disease
Medical therapy
Plane: Stress ECG  angiographs PCT
CABG-

88
Acute coronary syndrome
Unstable angina NSTEMI STEMI

- No ST elevation -No ST elevation - ST elevation
- neg cardiac enz - pos cardiac enz - pos cardiac enz
Unstable angina & NSTEMI

- Both have same symptoms & treatment
- Because we can't differentiate between them until no cardiac enzyme 12-18 hour
after symptoms
Clinical pictures: angina chest pain increase in severity frequency, duration

resistance to NTG
- May occur at rest
Diagnosis Abnormal ECG 1- ST segment deviation
1- EGG 2- new T wave inversion
Normal or minor changes
2- Cardiac enzyme - Unstable angina = Negative

-NSTMI = Positive
WHO criteria for
diagnosis ACS 2 of 3:
Treatment
Medical treatment 1-typical chest pain
1- Aspirin 2- ECG changes
2- ADP receptor antagonists:Clopidogrel (plavix) 3- Cardiac enzyme
positive
>> avoided in Pt will do CABG (Alternative:
Prasugrel ticagrelor)
3- antithrombin (Heparin) give until angiography
4-Glycoprotein IIb/IIIa: block platelets aggregation (TiroFiban, eptifibatide)
Side effects :bleeding, thrombocytopenia
4- Other: BB, NTG
5- Control diabetes
3- invasive management (CABG- PCI) (Recommended with 48 hours)

89
St Elevation MI
Clinical pictures:
1- Substernal diffuse pressure.
2- Radiate to neck, jaw, shoulder, and arm.
3- Accompanied with dizziness, nausea, vomited, diaphoresis, SOB.
4- Last > 20 𝑚𝑖𝑛
5- Not respond completely to NTG
6- Elderly & female : Atypical symptoms: nausea, dyspnea (silent MI)
Sign: 1- Pulse: Normal, bardycardiac (Inferior), Tachycardia (large)

2- Hypertension
3- S4
4 Paradoxically split Lt BBB.
Diagnosis
1- ECG :
a- ST Elevation ≥ I mm in 2 limb lead
b- ST elevation ≥ 2 mm in 2 chest lead
c- New Lt BBB

90
2- Cardiac enzyme Increase
Treatment
1- M: Morphine
O: O2
N: NTG Initial Management
A: Aspirin
2- Emergent reperfusion therapy
PCI with 90 min (better) OR Thrombolytic with 180 min
i- Thrombolytics:
1- Streptokinase + alteplase >>> Iv Infusion
2- Reteplase + Tenecteplase >> Rapid bolus
3- TPA most common
* Streptokinase should NOT used IF used with 12 month because antibodies.
Contraindications.
* Absolute
1- Acute bleeding, bleeding diathesis
2- Closed head, facial trauma within 3 month
3- Suspected aortic dissection
4- Prior intracranial hemorrhage
5- Ischemic stroke within 3 month
Relative contraindication
1- major surgery < 3week
2- Traumatic or prolonged. CPR
3- Recent (4week) internal bleeding
4- Active Peptic ulcer
5- Sever Uncontrolled HTN
6- Ischemia stroke < 3 𝑚𝑜𝑛𝑡ℎ.

91
Adjuvant therapy with reperfusion
Treatment PCI Thrombolytic
Antiplatelet
1- ASA + +
2-: Clopidogrel + 9_ 12 month + 1 month
Antithrombin + unfractionated
+
Heparin heparin bolus
-
Glycoprotein IIB IIIA + Bleeding,
thrombocytopenia
3- CABG. 1- FAILED PCI

2- Persistent or recurrent MI
Late presentation (> 12 ℎ𝑜𝑢𝑟 𝑎𝑓𝑡𝑒𝑟 𝑠𝑦𝑚𝑝𝑡𝑜𝑚𝑠)

If patient stable with No symptoms not recommended to do
PCI & fibrinolysis
Recommended discharge medication ACS

1- Aspirin
2-Clopidogrel: 9-12 month with stent
1 month with fibronlysis
3- BB: Metoprolol, carvedilol
4- ACE: If HEART Failure, stop later If improved
5- statin
6- NTG
7- warfarin: If A- Fib or mural thrombus
8 Control Risk Factor (HTN- DM)
Drug decrease mortality

1- statin 2- ASA 3- BB 4- CABG
Other testing in ACS.

1-Exercise ECG:
II- submaximal 4-7 day
II- Maximal 3-6 week
2- Myocardial perfusion Imaging: to assess extent of residual Ischemia

92
Complication ACS
1- Electrical disturbances
a- bradycardia: atropine or Pacing
b- Premature beats
c- supraventricular Tachyarrhythmia
d- ventricular Tachyarrhythmias (V-
Tach, V- Fib)
2- Conduction abnormalities
a- Block: First, second, third.
b- Intraventricular: bundle
branch block, hemiblock
3- Pump dysfunction
A- Contractile dysfunction: heart failure
B-mechanical disruption: MR, VSD
C- electromechanical dissociation
4- Ischemia
A- Post-infarction Ischemia
b- Recurrent Infraction
c- Post-infarction angina
5- pericarditis Dressler syndrome >> aspirin, NASID, steroids
6-Thromboembolic
a- Mural thrombus systemic embolism
b- DVT
7- Sudden Death
A- V-Fib (most common)
B- V-Tach
8- Rt ventricular Infarction with Inferior MI Give Fluids
Nonatherosclerotic ACS: (Prinzmetal, variant angina)

Spasm: of coronary artery
Clinical pictures:
Angina occur at rest at night or early morning
Terminates spontaneously
Diagnosis:
1- ECG ST elevation during attack
2- Stress test + angiograph Normal
3- ergonovine test confirmation
Treatment: 1- CCB 2- NTG

93
Note: During acute episode of Pain & ST segment elevation you can’t differentiate
variant angina from STEMI treat as STEMI
Causes of MI without Coronary A therosclerosis:
1- V as c u li t is
A. Sy s t em ic lu p us ery t h e ma t os us
B. P o ly ar t er it is n o dos a
C. Tak ay as u ar t er it is
D. M uc oc u ta n e ous ly m p h n od e s y n dr om e (K a was ak i)
2- A n o ma l ous or ig i n of c oro n ary ar tery
3- C or o n ar y s p as m
A. V ar ia nt an g in a
B. Coc a in e a b us e
4- C or o n ar y ar ter y em b o l us
A. Atr i a l my x o ma B. A tr ia l o r
v en tr ic u l ar t hr om b us
5- Hy per c o a gu l ab l e s t at es
A. P o ly c y t h e mi a v er a
B. Th r o m boc y tos is
C. Fac t or V L e id e n
D. Pr o te i n C d ef ic i enc y
E. A n ti p hos p h ol i p id an t i bo d i es
Congestive Heart Failure
-It is inability of the ventricle to efficiency Pump blood throughout the circulation.
- Compensatory mechanisms during HF
1- Cardiac: Frank – Starling, tachycardia, ventricular dilatation

2- Neuronal: - Increase sympathetic activity
-Decrease cardiac activity
3- Hormonal:- activation of Angiotensin –aldosterone system
- Vasopressin
- Catecholamines
- BNP
- Causes of Hf:
1- IHD 2- HTN
3- Cardiomyopathy 4- Valvular disease
5- congenital heart disease.
Note:
Most common cause of left side HF= IHD
Most common cause of right side HF = left sided HF

94
- Categorized of HF
1- Systolic Hf: Loss & contractile Strength & the heart (ejection fraction < 45%)
2- Diastolic HF: Loss of Relaxation of the heart (normal ejection fraction 60% +5)
3- Congestive HF: Rt side + Lt side HF
4- Decompensated HF: worsening symptoms of pre – existing HF: Due to

precipitating factor
1- MI 2- Infection (pneumonia)
3- arrhythmias (A-Fib) 4-increase salt at diet
5- Uncontrolled HTN 6- Thyrotoxicosis
7- Anemia 8- stop taking drugs ( most common)
-Symptoms of HF
RT side Lt side
1- Peripheral edema 1- Dyspnea
2- ascites 2- orthopnea
3- Jugular venous distention 3- Paroxysmal nocturnal dyspnea
4- Hepatomegaly 4- Fatigue – weakness
5-paroxysmal nocturnal dyspnea
-Classification of HF:
Class I: No limitation of activity
Class II : mild limitation of activity
Class III: Marked limitation of activity
Class IV: Confined to bed or chair.
- Diagnosis:
1- Echo: best test to confirm diagnosis
2- Chest x-ray
3- ECG.
4- BNP: Polypeptide secreted by heart in response to stretching >> evaluation of
decompensated heart failure
-Management:
* Systolic HF
1- Avoid precipitating factor: salt restriction, loss of body weight, do exercise,avoid
alcohol
2- Pharmacologic treatment :
A. diuretics (Furosemide) + vasodilator (ACEI)
B. Beta - blocker (carvedilol,metoprolol)

95
C. spironolactone
D. Intropics: Digoxin, dobutamine, dopamin, phosphodiesterase. Inhibitors
(amrinone: milrinore)
Note: dopamine, doputamine- phosphodiesterase, Inhibitor: Used in hospitalized

patient as Pt. need monitoring of blood pressure + cardiac rhythm
Note: - Monitoring of HF: 1- calculation & Fluid intake excretion

2- monitoring body weight
- refractory HF cannot respond to standard treatment need: Biventricular pacing.
Defibrillator, heart transplantation
* Diastolic Hf:
1- determine etiology
2- No Diuretics or vasodilator
3- BB or CCB.
4- May surgical correction
Medications:
1- Vasodilators:

96
2- Diuretics:
Thiazides Loop k-sparing
Furosemide (lasix) Spironolactone,

Hydrochlorothiazide
Ethacrynic acid, Eplerenone,
Examples chlorothiazide,
bumetanide, Amiloride,
Metolazone, indapamide
torsemide Triamterene
Distal tubule
Site of
Distal tubule Loop of henle (Aldosterone
action
antagonist)
4 hyper glucose 4 hypo
1-hyperglycemia 1-hypoNa
2-hyperlipidemia 2-hypoK
3-hyperuricemia 3- hypovolemia
4-hypercalcemia 4-hypoH+>>alkalosis 1-hyperK
Side effect 5-hypoCa for loop 2-gynecomastia for
spironolactone

97
3-Digitalis.
- Work on Na/K ATpase. Pump
- Decrease exchange Ca -Na
- Increase Ca + Inside cells
- result >> increase Force & velocity of
contraction
Uses & Digitalis

1- CHF
2- Atrid Fibrillation/ flutter
3- Paroxysmal arterial tachycardia
- Condition Increase digitalis toxicity.

1-Renal Insufficiency
2- Electrolyte disturbances: hypok, hypoCa, HypoMG
3- Old age 4- hypothyroidism 5- SA,AV BLOCK
Symptoms of Digitalis toxicity.

1- Nausea, vomiting
2- Gynecomastia
3- Blurred vision
4- yellow halo around objects
5- arrhythmias: PAT with block, PVCs, bradycardia
Treatment
1- Stop drug
2- lidocaine + phenytoin (arrhythmia)
3- digibind : anti digitalis antibodies in acute overdose
Note: Medication Lower mortality
1- ACE, ARAB
2- BETA BLOCKER
3- spironolactone
4- AICD
98
5- biventricular pacemaker
Pulmonary edema
Etiology : 1- Ischemia 2- arrhythmia 3- Non adherence with medication 4-

Dietary Indiscretion 5- Infection
Clinical Picture:
1- Respiratory Rate
2- Cyanosis
3- Cough with Pink Frothy sputum)
4- Nocturnal Dyspnea
5- rales-rhonchi wheel
Chest X-ray Finding

1- Prominent pulmonary vessels
2- Effusion
3- enlarged cardiac silhouette
4- kerley b lines
Treatment:
1- O2
2- Diuretics (furosemide)
3- morphine sulfate to decrease Respiratory
rate
4- Sitting patient upright
5- NTG
6- Digoxin
7- IV ACEI
Valvular heart disease
1- Mitral stenosis:
Etiology: 1- Rheumatic fever most common

2- congenital defect
Pathogenesis:
‫ ممييا يييإدي إلييى إرتجيياع الييد الييى الرئيية وزيييادة الض ي‬LA ‫ يحشيير الييد فييي‬mitral stenosis ‫فييي ال‬
‫ بسبب نقص كمية الد‬LSHF ‫ كما يحدث‬RSHF ‫ مما يإدي إلى‬RV ‫(وبعد مدة يزداد الض في‬plu/HTN)
LA‫ بسبب انحباس الد في‬Afib ‫ يحدث‬.‫التي تخرج من القلب‬

99
Clinical pictures:
1- Symptoms: RSHf + LSHF+ HHS
2-FATIGUE- Dyspnea
3- Orthopnea
4- Paroxysmal nocturnal dyspnea
5- Wasting
6- Hepatomegaly
7- ascites
8- Peripheral edema
9-J V P
10- Hemoptysis: Rupture of pulmonary vessels
11- Systemic embolism
12- Hoarseness of voice: (enlarged Lt Atrium compress the recurrent laryngeal nerve.
Sign:
1- Pulmonary rales
2- lowPulse pressure, sternal lift
3- Loud S1, Opening snap
4-Mid- Diastolic Rumble murmur in mitral
area
Diagnosis
1- ECG: RV, LA, RA, hypertrophy, A fib
may occur
2- Chest X ray: Large LA, pulmonary edema.
3- Echo: Thickening & mitral valve leaflets
4-LA enlargement
Treatment: 1- Diuretics - digitalis- salt restricted

2- anticoagulant >> A-Fib
3- Balloon valvulotomy
4- If fail all the above do mitral commissurotomy or valve Replacement

100
2- Mitral Regurgitation.
Etiology: 1- Ischemia Most common cause

2- HFN, CHF, rheumatic fever and any cause or left ventricular dilatation.
Pathogenesis : LV ‫ لكن يحدث تضخم للي‬MS ‫نفس ال‬

Symptoms: RSHF + LSHF
Sign:
1- Hyperdynamic displaced of LV.Impulse 5th to 6th intercostal space
2- Holosystolic murmur. On mitral area radiates to axilla with thrill.
3-S3, soft S1
Diagnosis
1- ECG: LV hypertrophy
2-Chest x-ray: cardiac enlargement (LV),
pulmonary edema
2- 3- Echo: Mitral valve prolapse + LV enlargement
4- Catheterization: most accurate (for all valves)
Treatment: 1- HF treatment: ACE, ARB, diuretics, Digitalis.

2- Mitral Valve Replacement. (Fail medical)
3- Mitral valve prolapse.
Etiology: Young women with connective tissue disease. (Marfan, Idiopathic)
Clinical picture: 1-asymptomatic

2- Palpitation, syncope, chest pain
Sign: 1- Mid to late click and late systolic murmur in mitral area
2- Increase With valsalva or standing.
3- Decrease with squatting
Complication: 1- arrhythmias 2- Sudden death- 3- CHF 4-

Endocarditis 5- TIA
Diagnosis: ECHO
Treatment:
1- NOt needed in most cases

101
2- BB for chest pain

3-Mitral Replacement
4- Aortic stenosis:
Etiology:
1- Aging most common cause.(calcified)
2- Congenitally Bicuspid Valve
3- Rheumatic Fever
Pathogenesis
‫ ويقل خروجه من القلب إلى الدماغ والشرايين التاجية وباقي الجسييم وبعييد فتييرة يرجييع الييد‬LV ‫الد بنحشر في‬
PLU HTN ‫إلى الرئة ويإدي إلى‬
Clinical Pictures
Symptoms:
1- Angina, syncope, dyspnea (CHF)
2- pulsus tardus et parvus (small low pulse)
Sign:
1-Harsh systolic murmur in aortic area (A1) Radiates to carotids with thrill
(crescendo decrescendo murmur)
2- S4, S2 Paradoxically split
Diagnosis:
ECG: LV Hypertrophy.
Chest x-ray: cardiomegaly, pulmonary edema.
Echo: thick aortic valve
Treatment: 1- Valve Replacement If area < 0.8 mm

2-Balloon if can’t replace the valve
Disease cause systolic murmur

- Aortic valve sclerosis in elderly
- Hypertrophic obstructive cardiomyopathy
- Mitral regurgitation
- Pulmonic stenosis
5-Aortic Regurgitation:
Etiology 1- HTN – Ischemia – Heart disease most common
2- Infective endocarditic
3- Syphilis 4- ankylosing spondylitis 5- rheumatic fever 6-aortic dissection 7-aortic
trauma
Pathogenesis:

102
‫ ونقصان الد الخارج من‬LV ‫ يرجع الد إلى القلب مما يإدي إلى تضخم في‬aortic regurgitation ‫في حالة‬
diastolic ‫ و‬systolic ‫القلب ونالحظ إنه سيكون فرق كبير بين ض‬
Plu / HTN ‫وبعد فترة يرجع الد إلى الرئة ويإدي‬
Clinical Pictures
-Symptoms: dyspnea most common
Sign:
1- Diastolic decrescendo murmur (typical) 3 Types of
2- Austin flint murmur murmur
3- systolic flow murmur
4- Peripheral sign of aortic regurgitation

• Corrigan’s pulse (water hammer pulse): A rapid and forceful distension of the
arterial pulse with a quick collapse
• De Musset’s sign: Bobbing of the head with each heartbeat (like a bird walking)
• Muller’s sign: Visible pulsations of the uvula
• Quincke’s sign: Capillary pulsations seen on light compression of the nail bed
• Traube’s sign: Systolic and diastolic sounds heard over the femoral artery (“pistol
shots”)
• Duroziez’s sign: Gradual pressure over the femoral artery leads to a systolic and
diastolic bruit
• Hill’s sign: Popliteal systolic blood pressure exceeding brachial systolic blood
pressure by ≥ 60 mmHg (most sensitive sign for aortic regurgitation)
• Shelly’s sign: Pulsation of the cervix
• Rosenbach’s sign: Hepatic pulsations
• Becker’s sign: Visible pulsation of the retinal arterioles
• Gerhardt’s sign (aka Sailer’s sign): Pulsation of the spleen in the presence of
splenomegaly
• Mayne’s sign: A decrease in diastolic blood pressure of 15 mmHg when the arm
is held above the head (very non-specific)
• Landolfi’s sign: Systolic contraction and diastolic dilation of the pupil
Diagnosis: 1- ECG: LV Hypertrophy

2- Chest x-ray: LV & Aortic dilation
3- Echo: dilated LV & aorta
Treatment
: 1-CHF treatment: salt restriction, diuretics, ACE, ARB, CCB.
2- Aortic valve Replacement in worsen symptoms or ejection fraction decease.
General rules to know.

103
All left side valvular disease- Increase- with Increasing blood to the heart except
‫والعكس صحيح‬mitral valve prolapse.
valsalva and standing = decrease blood to heart

Squatting and handgrip = increase blood to hear
Systolic murmur Diastolic murmur

Mid systolic : Early diastolic :
AS,PS,ASD,HOCM AR,PR,Austin flint
Holosystolic : Mid and late diastolic :

MR, TR,VSD MS,TS,graham-steel (murmur of PR)
Late systolic :
MVP
Continous (machinery) murmur : PDA, A-V fistula
Myocardial Disease
Cardiomyopathy: Disease involving heart muscle
1-Dilated congestive cardiomyopathy: most common cause for heart transplant

etiology
1- idiopathic: most common
2- alcoholic
3- peripartum
4- postmyocarditis due to infection
5- doxorubicin cyclophosphamide,
vincristine
6- Toxins (cobalt, lead, arsenic.)
7- Metabolic: hypoPO4, Hypok, HypoCa,
uremia
Clinical pictures: RSHF + LSHF

Diagnosis:
1- X-ray cardiomegaly + pulmonary congestion
2- ECG tachycardia + arrhythmias
3- Echo (diagnostic) dilated vertical
4- Catheterization
Treatment: as systolic HF.
2- Hypertrophic obstructive cardiomyopathy

- autosomal dominant triat on chromosome 14
104
- unexplained myocardial hypertrophy (usually interventricular septum)
pathophysiology:
(EF80- ‫عندما يتضخم القلب فإنه ال يمتلئى كامالً بالد وتكون إنقباضته قوية تإدي إلى تفريغ كل الييد بداخلييه‬
‫ فإن القلب يفرغ كل الد وبدون امتالء ما يإدي الى موت مفاجئ للمريض‬Tachycardia ‫وعندما يحدث‬90%)
Clinical pictures :
1- dyspnea, angina, presyncope,syncope,
palpitation
2- large Jugular A wave, S4, systolic
murmur and thrill
3- sudden death
Diagnosis:
- ECG: ventricular hypertrophy
- Echo: hypertrophy EF 80-90 %
Treatment:
1- BB, CCB
2- disopyramide
3- Implantable defibrillator if syncope
4- septoplasty in severe cases.
3- Restrictive Cardiomypathy. ( ‫(ال ينقبض وال ينبس‬

- Least common causes of cardiomyopathy.
Etiology:
1-infiltrative: sarcoidosis, amyloidosis,
Hemochromatosis, Neoplasia.
2- Scleroderma 3- Radiation
Note: hemochromatosis, Neoplasia is reversible
Pathophysiology: ‫يكون القلب عضلة صلبة ال تنقبض وال تنبس‬
Clinical Picture: Lt + Rt sides HF.

- Kussmaul sign: Jugular venous distention with
Inspiration
Diagnosis:
1- X- ray: Cardiomegaly + pulmonary congestion
2- ECG: Low voltage
3- Echo: Characteristic myocardial texture in Amyloidosis with thickening all cardiac
structure
4- Catheterization: square root sign.
Treatment:
- No good therapy
- Death for CHF
- Consider Heart transplantation
Note: as part of Catheterization is measure of atrium pressure

105
PERICARDIAL DISEASE
1- Acute pericarditis:
- Inflammation of pericardial lining around the heart
Etiology:
1- Idiopathic
2- Infection (Viral)
3- Vacuities (SLE)
4- Metabolic (Uremia)
5- Neoplasms
6- Trauma
7- Inflammation
Clinical Picture:
1- Chest pain localized substernally or to the left
2- worsened by lying down, coughing, deep Inspiration
3- Relieved by sitting up and leaning Forward.
4- Pericardial Friction Rub: (diagnostic) is scratchy high pitched sound. with 3
component, atrial systole, ventricular systole, early diastolic.
Diagnosis:
ECG: 1- ST Segment elevation all leads
2- Upright T waves.
106
3- PR segment depression
Treatment:
1- treating etiology
2- Idiopathic (NSAID, Aspirin corticosteroids)
3- colchicine decrease recurrence
2-Pericardial Effusion.
Accumulation of Fluid in pericardial cavity
Type Causes
Transudate. CHF, overhydration, hypoproteinemia
Exudate pericardial Injury
Serosanguineous TB- Neoplastic disease.
Blood Aortic aneurysm, aortic dissection, trauma.
Diagnosis:
1- ECHO: Fluid in echo- free Space.
2- Chest x- ray: water bottle.
Treatment:
1- Fluid aspiration
2- Treat the etiology
3- Cardiac tamponade
-It is life threatening condition in which percardial effusion developed rapidly or large
to compresses the heart
Etiology:
1- Neoplasia.
2- Idiopathic
3- Nonviral Infection: TB, suppurative.
4- Intrapericardial hemorrhage
5- surgery: chest, Heart, pericardium
6- Postpericardiotomy syndrome
7- Uremia
8 -Mediastinal Radiation therapy
9- Vasculitis.
Clinical pictures:
1- Dyspnea, Fatigue, orthopnea
2- Pulses paradoxus: decrease systolic blood pressure ≥ 10 with normal inspiration
3- Neck vein distension with clear lung
4- Shock (Hypotension)
107
5- Decreases Heart sound.

6- Beck's triad: I- low BP II- distended neck veins III-decrease heart sound
Diagnosis:
Clinical pictures + ECHO + Catheter (Show LA
+ RA equal pressures)
Treatment:
1-pericardiocentesis
2- subxiphoid drainage
4-Constrictive pericarditis:
- Diffuse thickening of pericardium in reaction
to prior inflammation
- Etiology:
1- Idiopathic
2- Following open heart surgery
3- Following thoracic radiation
4- Post viral infection
- Same us restrictive cardiomyopathy.
- Ct scan show thickened pericardium
- Treatment: Pericardiectomy

108
RATE AND RHYTHM DISTURBANCES

Disorder of sinus node function
1- Sinus bradycardia
QRS normal, Rate < 60 𝑚𝑖𝑛

Etiology:-
1- MI, diaphragmatic
2- Carotid sinus pressure
3- Vomiting
4- Valsalva maneuver
5- Depression of SA node, BB - CCB
6- Hypothyroidism
7- Marathon runner & swimming
8- Normal variant
Clinical picture: Syncope- Dizziness- weakness- Fatigue- SOB- chest pain -

confusion
Treatment:
1- No Necessary If no symptoms
2- Atropine (acute)
3- Pacemaker If symptoms persist
2- Av- Block
1- 1st degree block: PR > 0.20𝑠 ( ‫خمس مربعات‬
‫)ص ار‬
Etiology: 1- Aging
2- Digitalis
3- exaggerated vagal tone
4- Ischemia
5- Inflammation
6- Cardiomyopathies
Treatment: Not necessary

2- 2nd- Degree Block
1- Type 1- (mobitz I wenckebach)
2- (mobitz II)
Mobitz I Mobitz II
Etiology Degeneration in AV node Degeneration of His -
1- MI 2- Digitalis 3- RH purkinje system 1-MI
fever 2- Calcification of M+A
4- Myocarditis valve
109
site of block Av node Intra or Infra Hisian

ECG Progressive length & PR Sudden Drop beat without
Interval until Drop Beat change in PR interval
Then normal PR interval
Complication Escape Focus (Narrow QRS) Escape focus (Hide QRS)
2- Rate > 45 - Rate < 45
3- Adams Stroke uncommon - Adams stroke common
Treatment Not needed Need Pacemaker

3- 3rd- degree Block
atrium is beat alone- Ventricles beat by escape focus
Etiology: 1- Fibrosis of conduction system > Most common
2- A. spondylitis 3- Inferior, posterior MI 4- Infection 5- Digitalis
Clinical Picture: 1- Adam stroke attack, 2- CHF
Treatment: Pacemaker

110
supraventricular arrhythmia
1- Sinus Tachycardia:
- Rate > 100 beats 1 min
- Normal QRS regular
Etiology: 1- Fever 2- Hypotension 3- Anxiety 4- Pain 5- Discontinuation BB.
2- Paroxysmal supraventricular tachycardia.

(Paroxysmal atrial tachycardia.)
- Sudden onset & abrupt termination
- Regular Rhythm at Rate 130-220
beat/min
- Treatment:
1- Carotid sinus massage + ABCD.
2- A:adenosine: side effect >bronchoconstriction, half life 6 sec
3- B: Beta blocker
4- C: Calcium channels
5- D: Digitalis.
6- If pt Unstable (chest pain, SOB, Hypotension) > Synchronized external
cardioversion
3- multifocal atrial tachycardia:

- Multiple focus give multiple impulses
- Irregular Rhythm 100- 200 beats/ min
- 3 different P wave forms
- Common in chronic lung disease with
respiratory failure
Treatment: B- blocker, CCB(verapamil), digoxin
4- Atrial Flutter: (Regular Rhythm) (Saw tooth)
Etiology:
1- Chronic obstructive lung disease
2- Pulmonary embolism
3-Thyrotoxicosis
4- Mitral valve disease
5- Alchol.
Treatment: Digitalis, Verapamil, Beta Blocker

111
5- Artrial Fibrillation:
Etiology: 1- Rheumatic mitral valve.
2- CAD 3- CHF 4- HTN 5- Hyperthyroidism 6- Hypoxemia 7- Alcohol
Clinical Pictures:
1- Eldery patients 2- SOB 3- Dizziness 4- Palpitations 5- Acute Fatigue
6- Exacerbation of CHF
Diagnosis
1- History & Physical Ex, For duration & Frequency (Paroxysmal, presistan (First
episode), Precipitating Factor
2- ECG: Irregular rhythm with Fibrillatory waver (No p wave) + Check If there is Mi
3- Chest x-ray: For lung disease
4- Echo: to see If there is atrial thrombus
5- Thyroid function Test
Management:
* Ventricular Rate Control: decrease HR < 100 − 110

- BB, CCB, Digitalis. > Depends on patients medical condition & presence of Heart
Failure
BB. ‫ ال أستخد‬asthma ‫ وإذا كان عنده‬Digitalis ‫ بستخد‬HF ‫مثال إذا المريض عنده‬
* Mechanical Cardioversion: (electrical Shock)
- can be electively done to restore sinus rhythm but require sedation or anesthesia

112
- Can be given Immediately when the patient is unstable (acute heart failure,
hypotension, chest Pain)
- anticoagulation should be given.
* Pharmacolgic Cardioversion.
- Amiodarone, dofetilide, flecainide, Ibutilide,propafenone, quinidine
- Drug maintain sinus rhythm amiodarone, Disopyramide dofetilide, flecainide,
Propafenone, sotalol
* Catheter ablation: as most of Af Initiated by foci arise from 4 pulmonary veins can
be identified & eliminated
* Anticoagulation therapy: Accoring to CHADS.
C: CHF H: HYPERTENSION A: Age >75
D: Dm s: stroke or TIA
Each condition receives Point except stroke get 2
- PT with Chads O>>Aspirin
- Pt with Chads 1 >> Aspirin or warfarin
- Pt with CHADS 2- or more >> warfarins, dabigatran, rivaroxaban
*In clinical use, the CHADS2 score has been superseded by the CHA2DS2-VASc
score, which gives a better stratification of low-risk patients.
- CHA2DS2-VASc ( each 1 point except A and S is 2 point )
C: CHF H : Hypertension: blood pressure consistently above 140/90
mmHg (or treated hypertension on medication)
A2 : Age ≥75 years D : Diabetes Mellitus
S2: Prior Stroke or TIA or thromboembolism
V: Vascular disease A: Age 65–74 years
Sc: Sex category (i.e. female sex)
Wolff- Parkinson - white syndrome (wpw)
- It is pre- excitation of all or some portion of the ventricle by atrial impulses earlier
than normal impulses as there is accessory pathway (Kent bundle)
-ECG: short PR, wide QRS With slurred deflection, delta waves
- Associated with:
1- Paroxysmal supraventricular arrhythmia
2- Atrial Flutter, A-Fib
Treatment
1- IF pt unstable >> electrical cardioversion
2- If pt stable >> procainamide
3- Don't use: BB, CCB, Digoxin
4 Definitive treatment is ablation

113
Ventricular arrhythmias:
- Rate >
120 𝑤𝑖𝑡ℎ 𝑤𝑖𝑑𝑒 𝐵𝑖𝑧𝑎𝑟𝑟𝑒 𝑄𝑅𝑆.
- Etiology:
1- MI
2- Cardiomyopathies
3- Hypomagnesaemia., Hypoxia
4- Digitalis toxicity & Thioridazine
Clinical pictures:
1- Hypotension, CHF, SYNCOPE,
Cardiac arrests
2- Asynchronous atrial & ventricular contraction
3- Variation in systolic Blood pressure.

114
4- Variation in heart sound

5- Cannon A wave in Jugular venous pulses
6- Extra heart sound.
Treatment:
ACLS
Torsade de pontes.
Etiology Prolonged Qt:
1- Qunindine
2- Procainmide
3- Disopyramide
4- Psychotropic drug: 1- Phenothiaznes 2- Thioidazine. 3- TCA 4 -Lithium
5- Electrolyte Imbalance: hypok - hypo Mg
6- CNS: Subarachnoid, Interacerebral hemorrhage
Clinical Picture- Same V Tach

- Sudden auditory stimuli: Such as ringing telephone at night may initiate torsade de
point
Treatment:
1- If Pt unstable > Cardioversion
2- If PT Stable > lidocine.
3- Repletion of K, Mg

115
Ventricular Fibrillation
Etiology: 5 Hs + 5 Ts
1- Hypoxia 2- Hype/ Hype k 3- Hypothermia 4- hyperglycemia
5- Hypovolemia 6- Trauma 7- Toxins 8- Tamponade. 9- Tension pneumothrax.
10- Thrombosis
Clinical Picture:
dead person
Diagnosis: On ECG
Treatmente : ACLS

116
Differences between defibrillation & cardioversion

- Defibrillation: Non synchronized. Shock at any phase of cardiac cycle >> depolarize
all myocytes hoping SA hode start normal rhythm (used IN VF, Pulseless VT)
2- Cardioversion : Synchronized shock on QRS
Post - Resuscitation cure: If Pt not following commands or showing Purposeful

movement do hypothermia >> protocol to reduce anoxic brain injury (reach core
temperature 32- 34)
Asystole
Etiology
5H + 5T
Clinical Picture: unresponsive person with asystole ECG and no pulse
Diagnosis: Absence of electrical activity more than one lead.
Treatment= ACLS (CPR + Shock + vassoprossers)
Pulseless electrical activity

Etiology: 5HS + 5TS
Clinical Pictures: Patient dead with no pulse.
Diagnosis: Pulseless patient with normal activity on ECG
Treatment: ACLS (CPR + Vassoprossors)
DRUGS USED TO TREAT CARDIOVASCULAR

DISEASE
1- Amiodarone:
Side effect: 1- drug interaction
2-lung:cough,fever, painful breathing
3- CNS: change gait, tremor, numbness in finger and toes, dizziness,
muscle weakness
4- thyroid: hypothyroidism (common), hyperthyroidism
5- skin: sun burn, blue ray discoloration
6-eye: corneal deposits, halo light, blurred vision
2- Nitrates: ( isosorbide dibitrate , nitroglycerine , hydralazine , Nitroprusside )

117
Side effect: 1-orthostatic hypotension

2- tachycardia
3- throbbing headache
4-blushing
3-Beta blocker:
Side effect: 1- fatigue 2-mental depression 3-insomnia
4- adverse effect on lipid panel 5- hallucinations 6-Raynaud
phnomenon 7-bronchoconstriction 8-mask sign of hypoglycemia
9- sexual dysfunction
4-Calcium Channel blocker:

Side effect: (Cardiac): 1- CHF 2- réflex tachycardia 3-
hypotension 4- lightheadedness 5-AV node
Non cardiac: 1- flushing 2-headache 3-weakness

4-nausea 5-constipation 6-nasal congestion 7- wheezing
8- peripheral edema
Antiarrhythmic drugs
Drug Adverse Effects Mechansim
Disopyramid Anticholinergic effects; hypotension; heart failure;
e heart block; tachyarrhythmia
Lidocaine CNS (drowsiness, agitation, seizures); heart block
Phenytoin CNS (ataxia, nystagmus, drowsiness); hypotension
and heart block with rapid IV injection
Procainamide Lupus-like syndrome; GI; rash; hypotension;
aggravation of arrhythmia; blood dyscrasias
Quinidine Aggravation of arrhythmias (“quinidine syncope”);
thrombocytopenia; fever, rash; cinchonism; GI
symptoms; digoxin-quinidine interaction (elevation of
digoxin levels)
Na channel
Adenosine Transient dyspnea, noncardiac chest pain, rarely
hypotension blocker
Mexiletine Lidocaine-like drug; local anesthetic
Tocainide Lidocaine-like drug
Encainide Negative inotropism; QRS and PR prolongation
Flecainide Negative inotropism; QRS and PR prolongation
Propafenone Negative inotropism; QRS and PR prolongation
Amiodarone Very long half-life (20–40 d); may increase digoxin K channel
level; may worsen existing cardiac conduction blocker
disturbances; may prolong Coumadin effect
Beta-blocking Heart block; hypotension; asthma; hypoglycemia; Beta blocker
agents lethargy; impotence
Verapamil CHF, asystole, constipation Ca channel
blocker
118
Shock syndrome
Definition: imbalance between tissue oxygen supply and demand.
Types:
1- Distributive shock: caused by pathologic peripheral blood vessel vasodilation
- Examples are sepsis (especially gram-negative), anaphylaxis, neurogenic
- Septic shock is the most common form of shock among patients admitted to
theICU (followed by cardiogenic and hypovolemic shock)
2- Cardiogenic shock: related to impaired heart pump function

- Typical causes include acute coronary syndromes, valve failure (especially
acute) and dysrhythmias
3- Hypovolemic shock: caused by decreased circulatory volume

- Examples are hemorrhage (GI bleed) and fluid loss
4- Obstructive shock: non-cardiac obstruction to blood flow

- Examples are pulmonary embolus, tension pneumothorax, and cardiac
tamponade
Diagnosis: clinically
Note:
- In all of the forms above, cardiac output decreases; the only exceptions are
the hyperdynamic state of septic shock and rarely traumatic shock, both of which may
have elevated cardiac output.
Treatment:
1- ABC + intubation
2- O2
3- IV fluid
4- Blood transfusion
5- If not improved >> epinephrine, dopamine, vasopressin
6- Treat underlying cause: IV antibiotics for septic shock, thrombolysis for PE

119
‫‪Chapter 4 : Cardiology‬‬

‫‪120‬‬
HOW TO READ ECG

NORMAL ECG

121
DO N’ T m ent io n a ny 1- rhythm +rate

dia g no si s un t il y o u 2-Axis 3-II
rea c h t he e n d o f 4-V 1 , V 2 5-V 5 ,V 6
sc hem e COMPLETE ECG
1- Rhythm:
- regular or irregular (‫متساوية او غير متساوية‬RR ‫) المسافات بين‬
- source (sinus or not)
-rate: ‫ او عدد المربعات الكبيرة‬1500‫عدد المربعات الص يرة تقسيم‬
300 ‫تقسيم‬
2- AXIS: look for lead I & aVF
3- LEAD II: Wide, bifid >> LAE
P: Tall, peaked >> RAE

Saw tooth appearance >> A. Flutter
Irregular >>AF
Absent >> rhythum:
Regular>> nodal rhythum
PR interval: >> ‫ مربعات‬5 ‫ >>اكثر من‬AV 1 block

QRS: if Q wave also in lead III+ aVF transmural MI in the inferior surface then look
at St segment >> if raised “ recent “ if not “ old “
ST segment: >> depressed also in lead III +aVF >> ischemia. all lead >> digitalis or
hypoK
T wave: inverted also II + aVF >> ischemia … all leads >> late pericarditis
4- V1, V2 QRS shape: - if RSR – wide – inverted T wave)>> RT BBB

- If Q wave also in lead V2, V3, V4 >> MI antroseptal surface then look for ST
segment if rasied “ recent “ if not “ old “
Voltage: (normally rS)
Reversal (Rs) >> RVH Exaggerated (large rS) >> LVH
ST, T: As lead II
5- V5, V6 :QRS shape: - if RSR – wide – inverted T wave or monomophic R)>> LT
BBB
- If deep Q wave also in lead V5, I, aVL >> MI antrolatral surface then look
for ST segment if rasied “ recent “ if not “ old “
Voltage: (normally Rs)
Reversal (rS) >> RVH Exaggerated (large Rs) >> LVH
ST, T: As lead II
Note: if u diagnose case as LVH or MI then u find LTBBB >> diagnose as LT BBB

122
RHYTHM STRIP
IRREGULAR
QRS shape
Broad + Bizzare narrow, normal

P wave
Ventricular Present absent

Extrasystole
Supraventric 2AV block

may be : ilar
1- pulsus bigeminus Extrasystole
2- pulsus trigeminus A. Fib
3- pulsus quadrigeminus
close to each other << last 2 beat>> normal distance
____ << p wave >> present
REGULAR Bradycardia
QRS shape < 60
Bro a d + B izza r e Narrow, normal

P wave
3 AV
blo ck Present Absent or
inverted
Many>1 Only1
Nodal
Rhythm
3 AV 2 AV PR i nt erv a l
block block
prolonged
normal
1 AV
block Sinus
bradycharida
absent
>1P
Tachycardia >100
QRS shape
Narrow, normal
Bro a d + B izza r e
P wave
Ventricular Present absent
tachycardia
>1p Only1P
Supravent.
A.flu tt er tachycardia
Sin u s
tach y c ard i a

123
Common ECG findings

MI ST elevation, hyperacute T wave, pathological q wave
Angina ST elevation , T inversion , normal ECG
Variant angina ST elevstion (transient)
Post MI LV Presistant ST elevation 1 wk post MI
aneurysm
PE Sinus tachycardia, S1Q3T3
Pericarditis Diffuse ST elevation in all leads
Digoxin effect ST depression , T inversion, short QT interval
Digoxin toxicity PVCs, bradycardia
Hyperkalemia Peaked T wave, wide QRS, short QT , prolonged PR
Hypokalemia Flat T wave, Uwave
Hypercalcemia Short QT interval
Hypocalcemia Long QT interval
LAH Bifid P wave
RAH Peaked P wave
A.flutter Saw tooth P wave
A-Fib No P wave , irregular , narrow QRS
SVT No P wave, regular, narrow QRS
V. Tach HR > 250 , wide QRS
Myocarditis / Prolonged PR interval
rheumatic fever
MS A-fib , bifid P wave , RVH, RAD
MR A-fib , bifid P wave , LVH, LAD
AS Bifid P wave , LVH, LAD
AR LVH,LAH (bifid P wave )
WPW Short PR, delta wave , wide QRS
Torsades de point Polymorphic V.tach
Hypothermia Bradycardia , long QRS, Osborne J wave (hump like )

124
Chapter 5
Hematology

125
‫‪Chapter 5 : Hematology‬‬

‫‪126‬‬
ANEMIA
Defin it io n s :
1- Hem a to cr it : ‫نس به كري ا ت ا ل د ال حم ر اء في ا لد‬

2- Seru m ir o n : t r an sf er r in ‫كمي ه ال حد يد ا لمرت ب م ع‬
3- Ferr it ien : ‫صي ه ال حد ي د ا لم خ ز ن في ال د‬
4- TIB C : tr an sf e r r in ‫قا ب لي ه ار تب اط ا لح دي د م ع‬
5- RD W : ‫معد ل اال خت ال ف في حجم ك ر يا ت ال د ال حم ر اء‬
6- MC V : ‫ح جم ك ري ا ت ا لد ال حم راء‬
7- MC H : ‫كم يه ا له يموغ لو ب ي ن ب ك ريا ت ا لد ا لحم را ء‬
8- MC H C : ‫تر كيز ا لهي موغ لو بي ن في ك ري ا ت ا لد ال حم ر اء‬
Definition :- hematocrit (Hct) <41%in men / <36%in women

OR
- hemoglobin <13.5 gm/dl in men / <12 gm\dl in women.
Etiology:
1- microcytic anemia (MCV<80 ): iron deficiency, thalassemia, sideroblastosis, lead

poisoning,anemia of chronic disease
2- Macrocytic anemia (MCV >100) : vitamin B12 , folic acid deficiency, alcohol,
liver disease, chemotherapeutic, medication
3- Normocytic anemia :hemolysis.
Clinical pictures :
‫منحطهم‬
- Early symptoms : fatigue, tiredness, poor exercise tolerance.
‫في كل‬
- Next symptoms :dyspnea on exertion, lightheadedness. anemia
- Late symptoms :confusion, altered mental status.
Diagnosis :
CBC, MCV,Iron studies, reticulocyte count, peripheral smear, red cell distribution of
width (RDW),coombs test, vitamin B12 + folate levels, bone marrow biopsy.
Treatment :
- blood transfusion ( packed red blood cells )

- keep Hematocrit >20% in healthy young and > 30 % in older patient
- Hematocrit rise 3 points every unit of packed red blood.

127

‫‪128‬‬
MICROCYTIC ANEMIA
Iron Deficiency Anemia

NOTE: daily requirements of iron :
Etiology:.
Man: 1 mg/ day iron
- blood loss from GIT or
menstruation. Woman :2-3 mg / day iron
- increase demand : pregnant, Pregnant: 5 -6 mg / day
puberty Maximum absorption 3 -4 mg / day so
- urinary loss of blood pregnant will have i ron deficiency
- malabsorption
anemia
- hemolysis
- poor oral intake.
Clinical pictures:
1- hematologic symptoms
2- specific symptoms to iron deficiency:
- brittle nails
-spoon shaped nails
-glossitis
- pica
Diagnosis:
- low serum ferritin,MCV, serum iron
- high TIBC
- high RDW
- high platelet count
- low reticulocyte count
- bone marrow biopsy: Most specific test looking for stainable iron stores
Treatment:
- ferrous sulfate tablets: most common
used until Hb and Htc normal and Side effect of ferrous sulfate :
additional 2-3 months to fill iron
- Abdominal discomfort
stores
- Nausea
- IV iron: for malabsorption
- Diarrhea / constipation
- blood transfusion is the most effective
- Black tarry stool
method

129
Anemia of chronic Disease
Etiology:
- hepcidin (regulator of iron metabolism) is abnormally high in any chronic disease
- iron trapped within macrophages and liver cell and decrease gut iron absorption
Clinical pictures: hematologic symptoms.
Diagnosis:
- Serum ferritin is normal or elevated
- serum iron level + (TIBC) are low.
- reticulocyte count is low
Treatment:
- Correct the underlying disease
- Iron supplementation and erythropoietin in renal disease and anemia caused by
chemotherapy or radiation therapy
Sideroblastic Anemia
- disorder in the synthesis of hemoglobin characterized by trapped iron in the
mitochondria of nucleated RBCs.
Etiology:
1- hereditary:
a. defect in aminolevulinic acid synthase
b. abnormality of vitamin B6 metabolism
2- acquired: chloramphenicol, isoniazid, alcohol, Lead poisoning myelodysplastic
syndromes
Clinical pictures : hematologic symptoms.
Diagnosis:
1- high serum ferritin + serum iron
2- low TIBC,
3- prussian Blue stain:. most specific test will
show the ringed sideroblasts.
Treatment :
- stop offending drug
- Treat the lead poisoning
- pyridoxine therapy 2 -4 mg per day.

130
Thalassemia Type of Hg :
Etiology: 1- A 1 : 2 alpha + 2 Beta
- Gene deletion for genes coding to globin chain 2- A 2 : 2 alpha + 2 delta
- 4 genes coding for the alpha chain of the 3- F: 2 alpha + 2 gamma
hemoglobin on chromosome 16.
- 2 genes for Beta chain on chromosome 11
- Alpha thalassemia common in Asian populations Beta thalassemia common in
Mediterranean populations.
Clinical Pictures: (depend on number of gene deleted)

1- alpha thalassemia:
a- 1 gene deleted : CBC,hemoglobin, MCV are
normal
b- 2 genes deleted :mild anemia, hematocrits 30
– 40 %, low MCV.
c- 3 genes deleted: sevre anemia, hematocrits 22-
32 %,very low MCV
d- 4 genedeleted: die in utero.
2- Beta thalassemia
I- major (cooley anemia):
- symptoms starting at 6 month of age when the body switch from fetal hemoglobin to
adult hemoglobin
-growth failure
- hepatosplenomegaly, jaundice
- bony deformities secondary to extramedullary hematopoiesis.
- symptomatic hemochromatosis, cirrhosis,congestive heart failure from chronic
anemia and transfusion dependence.
II- triat : mild anemia
Diagnosis :
1- microcytic anemia with normal
iron studies.
2- Hemoglobin electrophoresis tells
which type
3- RDW is normal.
Treatment:
1- blood transfusions once or twice a
month
2- deferasirox (oral), deferoxamine
(subcutaneous pump)
3- Splenectomy reduce transfusion requirements.
4- bone marrow transplantation.
131
MACROCYTIC ANEMIA
Vitamin B12(Cyanocobalamine)Deficiency
Etiolgy:
1- Pernicious anemia (decreased intrinsic factor production on an autoimmune
basis).
2- Gastrectomy, atrophic gastritis
3- Malabsorption: sprue, regional enteritis, blind loop syndrome
4- Pancreatic insufficiency
5- tapeworm :Diphyllobothrium latum.
Clinical Pictures:
1- hematologic manifestation: as above
2- Neurologic manifestations :peripheral neuropathy, position sense
abnormality,vibratory, psychiatric, autonomic, motor, cranial nerve, bowel,
bladder and sexual dysfunction. Glossitis, diarrhea, and abdominal pain
hematologic deficits.
Diagnosis:
1- high MCV
2- white blood cells have hypersegmented
neutrophils
3- RBCs macro-ovalocytes.
4- Low Reticulocyte
5- bone marrow is hypercellular.
6- pancytopenia
7- High LDH, bilirubin,iron level may occur but are nonspecific.
8- low B12 level: Most specific
9- Antibodies to intrinsic factor and parietal cells confirm the etiology as pernicious
anemia.
10- schilling test is rarely used.
11- High methylmalonic acid level.

132
Treatment:
- vit B12 replacement (oral, IM, subcu)
- IV not recommended because the vitamine will lost in urine
- hypokalemia and fluid overload can result from vit B12 replacement
Folic Acid Deficiency
Etiology: Antifolate drugs:

1- decreased dietary intake
2- increased requirements >>pregnancy, - Phenytoin
3- skin loss in diseases like eczema, - Valproic acid
4- increased loss from dialysis, anticonvulsants as - Methotrexate
phenytoin - Trimethorprim
5- Alcoholics: alcohol inhibits conjugase enzyme
Clinical pictures : hematologic symptoms
Diagnosis: low RBCs, low folic acid level.
Treatment : Replace folic acid, orally.
HEMOLYTIC ANEMIA
Etiology:

133
Clinical pictures:
- Symptoms of anemia as described above
- Symptoms of hemolysis:Jaundice,dark urine, ‫منحطهم في كل ا نواع‬
- fever,chills, chest pain, tachycardia, backache hemolytic anemia
Diagnosis:
1- normal MCV
2- high reticulocyte, ‫منحطهم في كل ا نواع‬
hemolytic anemia
3- high LDH, indirect bilirubin
4- low haptoglobin.
Treatment.Transfusion,Hydration,Specific therapy with each disease below.
Sickle Cell Disease
Etiology. autosomal recessive hereditary disease with substitution of a valine for

glutamic acid as the sixth amino acid of the beta globin chain >> Hg S
- sickle cell disease (HBSS) >> homozygous >> symptomatic

- sickle cell triat (carrier)(HBAS)>> heterozygous >>asymptomatic (just UTI,
isosthenuria)
Clinical Pictures:
Chronic symptoms:
- isosthenuria, hematuria
- ulcerations of the skin of the legs
- bilirubin gallstones
- aseptic necrosis of the femoral head,
osteomyelitis
- retinopathy
- recurrent infections from pneumococcus or Haemophilus,
- growth retardation,
- splenomegaly followed in adulthood by autosplenectomy
Acute symptoms:
- acute painful crisis consists of back, rib, chest, and leg pain,

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- Acute chest syndrome consisting of severe chest pain, fiver, leukocytosis, hypoxia,
and infiltrates on chest x- ray
- Stroke and TIA.
- priapism prostatic plexus of veins infarction.
- Blindness even myocardial infarction and cardiomyopathy may also occur.
- Pregnant: spontaneous abortion, low birth weight
Sickle trait:
- Isosthenuria and microscopic Hematuria

- UTI
Diagnosis:
1- As all hemolytic anemia (normal MCV, high reticulocytes, LDH …etc)
2- hemoglobin electrophoresis is the most specific test.
3- peripheral smear shows sickled cells
4- sickle prep (or Sickledex) is a quick screening test
5- Urinalysis: microscopic Hematuria
6- WBCs often elevated in the 10,000 – 20,000 with infection.
Treatment:
acute sickle cell pain crisis

- fluids, analgesics, oxygen,Antibiotics (Ceftriaxone)
- Severe or life - threatening manifestations :exchange transfusion (high Hct) or
RBc transfusion (low Hct)
Chronic management:
- folic acid replacement
- vaccinetions against pneumococcus and influenza
- Hydroxyurea
- bone marrow transplantation.
Autoimmune, Cold Agglutinin, and Drug – Induced Hemolytic

Anemia.
- production of IgG, IgM, or activation of complement C3 against the red cell
membrane
Etiology:
Autoimmune:
- idiopathic
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- viral infections,
- lymphoma
- collagen vascular diseases lupus
- Ulcerativ colitis.
Drugs:
- penicillins, cephalosporbins, sulfa drugs, quinidine, alphamethyldopa, procainamide,
rifampin, and thiazides.
Cold agglutinin: IgM antibody produced against the red cell in association with
1- malignancies as lymphoma or Waldenstrom macroglobulinemia
2- infections such as Mycoplasma.
Clinical Pictures:
1- hematologic symptoms
2- symptoms of hemolysis
3- fever, syncope, congestive failure, hemoglobinuria.
4- Mild splenomegaly
5- cold agglutinin in cyanosis of the ears, nose, fingers, and tose.
Diagnosis :
2- coombs test specific test
3- Spherocytes on the smear.
Treatment:
1- Mild disease no treatment.
2- stop the offending drug.
3- Sever hemolysis >>steroids >> if fail >> Splenectomy.
4- Cold agglutinin avoiding the cold.
5- azathioprine, cyclosporine, or cyclophosphamide.
6- Rituximab.
Note: steroid and splenectomy not working with cold agglutinin

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Hereditary Spherocytosis:
Etiology :autosomal dominant >>loss of spectrin in the red cell membrane.
Clinical Presentation:
1- Hematologic symptoms
2- Symptoms of hemolysis
3- Splenomegaly
Diagnosis:
2- negative Coombs test
3- osmotic fragility test
4- high (MCHC).
Treatment:
1- Folate replacement
2- severe anemia: removal of the spleen.
Paroxysmal Nocturnal Hemoglobinuria (PNH)
Etiology:
- RBC membrane defect in phosphatidyl inositol glycan A (PIG-A) >>binding of
complement to the red cell >> intravascular hemolysis.
- More susceptible to lysis by complement in an acid environment >> at night
because of a relative hypoventilation.
Clinical Pictures:
1- Hematologic symptoms
2- dark urine in the morning form intravascular hemolysis at night.
3- Thrombosis of major venous structures (Budd-Chiari syndrome).
Diagnosis:
2- sugar – water test
3- the acidified – hemolysis (Ham) test specific tests
4- Decay accelerating factor (DAF)(CD55) (CD59).
Treatment:
1- Folic acid +Iron replacement
2- Corticosteroids
3- Anticoagulation >> for Thromboses.
4- Eculizumab >> inhibits complement.

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Glucose -6-Phosphate Dehydrogenase (G6PD) Deficiency
Etiology: hereditary disease lead to

deficiency of enzyme (G6PD) that
neutralizing oxidant stress to RBCs
Oxidant stress:
1- infections
2- drugs: sulfa drugs primiquine,
dapsone, quinidine, and nitrofurantion.
Clinical Pictures:
1- pt normal until exposed to stress
2- when exposed to stress:sudden, severe, intravascular hemolysis >> jaundice,
dark urine,weakness, tachycardia.
Diagnosis.
2- Blood smear >>Heinz bodies,Bite cells
3- G6PD level >> 1 week after the event
(specific test)
Treatment:
1- hydration and transfusion main therapy
2- avoid oxidant stress in the future.
APLASTIC ANEMIA
- failure of all 3 cell ines (RBCs, WBCs, platelet) >> pancytopenia
Etiology:
1- idopathic: most common
2- Radiation
3- toxins such as benzene
4- Drugs: NSID, choramphenicol, alcohol, chemotherapeutic alkylating agents
5- Infiltration of bone marrow: TB, lymphoma
6- Infection:hepatitis, HIV, CMV, Epstein Barr virus, parovirus B19
Clinical Pictures:
1- bleeding from thrombocytopenia
2- fatigue from anemia
3- infections from neutropenia
Diagnosis:
1- CBC >> Pancytopenia.

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2- A bone marrow biopsy >>empty hypoplastic and fat filled with no abnormal
cells seen.
Treatment:
Bone marrow transplantation >> if not possible >> antithymocyte globulin,
cyclosporine and prednisone.
ACUTE LEUKEMIA
Etiology :
1- radiation exposure
2- benzene
3- chemotherapeutic agents such as
melphalan
4- retroviruses
5- Down syndrome and Klinefelter
6- Myelodysplasia and
sideroblastic.
Clinical Pictures:
1- bleeding from
thrombocytopenia
2- fatigue from anemia ( most
common )
3- infections from neutropenia
4- Enlargement of the liver, spleen, lymph nodes, bone
5- (DIC)is associated with M3
6- CNS involvement (meningitis):M4 and M5
7- syndrome of ‘leucostasis’: high WBCs >>headache, dyspnea, confusion, brain
hemorrhage.
Causes of pancytopenia :
1-Leukemia 2-aplastic anemia 3-infections involving the marrow

4- metastatic cancer involving the marrow 5-vitamin B12
deficiency 6- SLE 7-hypersplenism, 8-myelofibrosis.
Diagnosis:
1- CBC: pancytopenia
2- bone marrow biopsy >> showing > 20% blasts
3- AML marker: Auer rods, myeloperoxidase, and esterase
4- ALL marker:common ALLantigen (CALLA) and
terminal deoxynucleotidyl transfer-(TdT).
5- monoclonal antibodies test: recognize the specific types

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6- hyperuricemia
7- highLDH.
Treatment.
1- Chemotherapy:
- AML >> cytosine arabinoside (AraC) +
daunorubicin or idarubicin.
- ALL >>daunorubicin, vitcristine, prednisone.
2- Leucostasis >> leukapheresis.
3- After chemotherapy >>bone marrow
transplantation
ALL patients need prophylaxis of the central

nervous system with intrathecal methotrexate.
CHRONIC LEUKEMIA
Chronic Myelogenous Leukemia (CML)
- massive overproduction of myeloid cells.
Etiology :
- Philadelphia chromosome translocation between chromosomes 9 and 22 >>gene
producing an enzyme with tyrosine kinase activity.
Clinical Pictures:
1-night sweats
2-low grade fever
3-Abdominal pain from massive enlargement of spleen is common.
4-Bone pain from infiltration with WBCs.
5-Infection and bleeding are uncommon
6-leukostasis >> Dyspnea, blurry vision, priapism, thrombosis, stroke
Diagnosis:
1- high WBCs (200000-500000 )
2- Low or absent Blasts <5%.
3- Low Alkaline phosphatase score (LAP).
4- High B12 level
5- philadelphia chromosome: specific test
6- high Platelet.
Note:
- CML can be confused with a leukemoid reaction.They are distinguishable based
upon the leukocyte alkaline phosphatase (low in CML).
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Treatment: imatinib >> if fail >> bone marrow transplant.
Chronic Lymphocytic Leukemia (CLL)
Overproduction of mature, but still leukemic, lymphocytes (B cells)
Etiology: unknown.
Clinical Pictures:
- asymptomatic elevation of white cell found on routine evaluation of patients or
during investigations for other problems.
- Fatigue, lethargy,and uncomfortable enlagement of lymph nodes
- Infiltration reticuloendothelial system: spleen, liver, and bone marrow
Staging for CLL is

• Stage 0,lymphocytosis
• Stage 1,lymphadenopathy 10 – 12 year
• Stage 2,splenomegaly 5 year
• Stage 3,anemia
• Stage 4,thrombocytopenia 1-2 years
Diagnosis:
1- High WBCs (lymphocyte) 30000-50000
2- “ Smudag cells “ seen on a smeara
Treatment:
- Early stage:not treated
- Advance stage: fludarabine, prednisone,Rituxomab
Hairy Cell Leukemia

- Subtypes of CLL
- Malignant B lymphocytes (hairy cell) accumulate in the bone marrow lead to
pancytopenia
- Diagnosed by bone marrow biopsy with special stain TRAP
- Treated by: cladribine, pentostatin, rituximab, interferon

141
Myelodysplasic Syndrome (MDS)
Etiology: Pre – AML form a genetic defect
Clinical pictures: pancytopenia >>fatigue,

infection, bleeding
Diagnosis:
1- CBC and bone marrow find a bi- lobed
neutrophil called a pelgerHuet cell
2- Genetic testing for the 5q- deletion is
essential
Treatment :
- TNF inhibitor: lenalidomide or thalidomide
- Azacitidine or decitabine
- bone marrow transplantation.
Polycythemia Vera (primary)

Definition :Red cell are produced in excessive amounts
in the absence of hypoxia or increased erythropoietin levels.
Secondary polycythemia :
Clinical Presentation
* Markedly elevated hematocrit 1- Hypoxi
* Splenomegaly - COPD
* Sometimes elevation of the platelet and - Hypoventilation: obesity,
white cell counts pikwikian syn
* Thromobosis - High altitude living
* ” plethora” or redness and fullness of the - Cyanotic congenital heart
face. disease
2- High erythropoietin
Diagnosis. - Renal cell CA
1- High hematocrit - Hepato cellular CA
2- Janus Kinase or JAK-2: most specific test. - Uterine fibroma
Treatment : - Androgen hormones
1- phlebotomy
2- Hydroxyurea
3- aspirin to reduce risk of thrombosis
Essential Thrombocythemia :
- Cancer of platelet >>Platelet over million
- Lead to bleeding or thrombosis
- JAK-2 most specific test
- Treated by hydroxyurea and anagrelide

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Causes of thrombocytosis:
1- Essential thrombocytosis 2- CML 3-polycythemia vera
4- RA 5- post splenectomy 6- stress: trauma, surgery
7- inflammation: sepsis 8-kawazkie disease
9-henoch- schnolein purpura
Note: RA cause thrombocytos is while SLE cause thrombocytopenia
PLASMA CELL DISORDERS

Multiple Myeloma
Definition: a bnormality of plasma cell resulting in their overproduction replacing the

marrow as well as the production of large quantities of functionless immunoglobulins.
Etiology: unknown.
Clinical pictures:
1- Bone pain (back, ribs) secondary to pathologic fractures.( most common )
2- Radiculopathy
3- Infection encapsulated organ isms such as pneumococcus and Haemophilus
4- Renal failure
5- anemia
6- hypercalcemia >> polyuria, polydipsia, and altered mental status
7- Weakness, fatigue and pallor blurry vision, confusion, and mucosal bleeding may
occur.
Diagnosis:
1- normochromic normocytic anemia
2- protein electrophoresis: monoclonal immunoglobulin IgG.
3- plain x-ray punched-out lytic lesion,
4- Hypercalcemia
5- high BUN and creatinine
6- bone marrow biopsy greater than 10% plasma cell confirms a diagnosis
7- specific test for Bence – Jones protein involving acidification of the urine
Treatment :
1- bone marrow transplantation.
2- melphalan and prednisone.
3- Hypercalcemia hydration and loop diuretics
4- Bortezomib proteasome inhibitor.

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Monoclonal Gammopathy of Uncertain Significance(MGUS)
Definition overproduction of a particular immunoglobulin by plasma cells without the

systemic manifestations.
Etiology: unkown.
Clinical Pictures. no symptoms
Diagnosis:
1- protein electrophoresis high monoclonal immunoglobulin
2- elevated total serum protein the clue to the diagnosis
Treatment. not necessary
LYMPHOMA
Hodgkin Non hodgkin
Pathlogy reed strenbrug cell no reed strenbrug cell
Etiology no factor HIV,EBV,HCV,H.PYLORI
Symptoms - paniless rubbery - paniless rubbery
nontender non erythmatoses nontender non erythmatoses
cervical, axillary, supraclvicular LN
LN
- B sym(fever, wieght loss, - B sym(fever, wieght loss, nieght
nieght sweats) sweats)
- pruritius - pruritius
- extralymphatic (less common) - extralymphatic more common
Diagnosis EX LN biopsy Same but the extralymphatic more
CT MRI common
PET scan
CBC(anemnia,esinophilia)
LDH LFT
Treatment radiation (1, 2) radiation (1,2)
chemo (3,4) ABVD MOPP chemo (3,4) CHOPP
rituximab
Staging Stage 1: 1 lymphatic group or single extra lymphatic site
Stage 2: 2 lymphatic groups or extra lymphatic sites on 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 bone marrow or liver

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Tumor Lysis Syndrome

- oncologic emergency caused by massive tumor cell lysis
- most common after initiation of Cytotoxic therapy for leukemia and lymphoma
- cause hyperuricemia, hyperphosphatemia, Hyperkalemia, hypocalcemia
- uric acid precipitates in the renal tubules lead to acute kidney injury
- patient should receive prophylactic allopurinol, IV fluid with chemotherapy
- Rasburicase is alternative to allopurinal
- Alkalization of urine is controversial

145
BLEEDING DISORDERS
PLATELET DISORDERS
Immune Thrombocytopenic Purpura (ITP)

Etiology: idiopathic production of an antibody to the platelet, platelets are bound
macrophage and brought to the spleen.
Clinical Pictures:
- bleeding from superficial areas of the
body: skin, nasal and oral mucosa, GIT,
urine, vagina.
- epistaxis
- Petechiae, purpura, ecchymoses,
bruising
- hematuria
- dysfunctional uterine bleeding
- Splenomegaly shoud be absent.

146
Diagnosis:
1- Thrombocytopenia.
2- Antiplatelet antibody have a high sensitivity
3- bone marrow megakaryocytes.
Causes of thrombocytopenia
Increase platelet destruction Decrease platelet production
1- microangiopatic hemolytic anemia: 1- infiltration of BM:
DIC, TTP, HUS, HELP syndrome TB,lymphoma, leukemia
2- autoimmune: TIP,HIT syndrome, 2- Aplastic anemia
SLE 3- Myelofibrosis
3- drugs: digoxin, heparin …etc 4- Sever megaloblastic anemia
4- hypersplenism
Treatment :
1- Predinisone is the initial
2- Splenectomy for low platelet counts 10,000 – 20,000 / mm.
3- IVIG or RhoGAM™ (<10,000)μL or in life - threatening bleeding.(for Rh-
Positive patients).
4- thrombopietin agents romiplostim or eltrombopag, Rituximab.
Von Willebrand Disease (vWD)

Etiology:
- autosomal dominant
- the most common congenital disorder of hemostasis
- loss the ability of platelets to adhere to the endothelial lining
Clinical Pictures:
1- Mucosal and skin bleeding such as epistaxis, petechiae, bruising,
2- menstrual abnormalities.
3- gastrointestinal and urinary tract bleeding.
Diagnosis:
1- normal platelet
2- bleeding time high.
3- low level of von willebrand factor, also known as factor VIII antigen.
4- ristocetin platelet aggregation test,abnormal.
5- PTT elevated.
Treatment.
1- Desmopressin acetate
2- factor VIII replacement.

147
COAGULOPATHY
Hemophilia A and B
- Factor VIII deficiency in hemophilia A

- factor IX deficiency in hemophilia B
Etiology : X-linked recessive disorders

Clinical Pictures:
1- Mild deficiencies: no symptoms or only during
surgical procedures or trauma.
2- severe deficiencies : spontaneous bleeding,
deeper than that produced with platelet disorders
>> hemarthrosis, hematoma, gastrointestinal
bleeding, or urinary bleeding, Bruising and
central nervous system bleeding can also
3- Bleeding at the time of circumcision.
Diagnosis ;
1- Prolonged PTT
2- normal PT
3- 50:50 mixture “mixing study”
4- Specific factor VIII or IX levels
Treatment:
- desmopressin
- replacement of the specific factor.
Vitamin K Deficiency
- vitamin K >>factor II, VII, IX,X = 1972
Etiology: dietary deficiency, malabsorption,antibiotics that kill the bacteria in the

colon
Clinical Pictures: same hemophilia
Diagnosis:
1- PT and PTT are elevated
2- correction of the PT and PTT in response to giving vitamin K
Treatment :Severe bleeding fresh frozen plasma +Vitamin K

148
Liver Disease
Etiology : Liver disease or cirrhosis
Clinical Pictures: Bleeding from any site,but the GIT is the most common site.
Diagnosis :
- PT and PTT no improvement when vitamin K is given.
- clear history of liver disease
- .low platelet count
Treatment: Fresh frozen
Disseminated Intravascular coagulation (DIC)

Definition Consumptive coagulopathy resulting in consumption both platelet and
clotting factor type and occasionally thrombosis may be acute or chronic (most in
cancer)
Etiology
1- idiopathic
2- rhabdomyloysis
3- adenocarcinomas
4- heatstroke
5- hemolysis from transfusion reaction
6- burns, head trauma
7- obstetrical disasters such as abruption placenta and amniotic fluid embolism
trauma,
8- Pancreatitis, snakebites.
9- Gram negative sepsis
10- Promyelocytic leukemia (M3)
Clinical Picutres:
1- Bleeding from any site in the body.
2- Hemolysis
3- renal failure, jaundice and confusion.
Diagnosis:
1- High both the PT and PTT
2- low platelet count,
3- low fibrinogen levels
4- . D- dimmers and fibrin >> split products are present in increased amounts
5- blood smear shows schistocytes as fragmented cells consistent
Treatment
- severe bleeding, fresh frozen plasma (FFP) and sometimes platelet transfusions
149
- Heparin is controversial.
- correct the underlying disorder
Thrombotic Thrombocytopenic Purpura / Hemolytic Uremic Syndrome
TTP:
Etiology:
- idiopathic inhibition of ADAMTS13 enzyme which responsible of cleaving of VW
factor
- increase vWF increase platelet adhesion to areas of endothelial injury
- secondary TTP result in: cancer, HIV, drugs (ticlopidine, clopdigrel, cyclosporine)
clinical pictures:
- hemolytic anemia, uremia, thrombocytopenia, fever and neurologic problems
Diagnosis:
- CBC: anemia, thrombocytopenia
- High BUN, Cr
- High LDH, bilirubin, reticulocyte
- Low haptoglobin
- Blood smear: shistocytes, helmet cell, fragmented RBCs
Treatment:
- Plasmapheresis
- Dipyridamole
- Don’t transfuse platelets
HUS:
Etiology:
- Shiga like toxin produced by: Ecoli, campylobacter, shigella
Clinical pictures
- Hemolytic anemia, uremia, thrombocytopenia
Diagnosis:

150
- CBC: anemia, thrombocytopenia

- High BUN, Cr
- High LDH, bilirubin, reticulocyte
- Low haptoglobin
- Blood smear: shistocytes, helmet cell, fragmented RBCs
Treatment:
- Mild disease resolves spontaneously
- Sever disease >> plasmapheresis
- Don’t give antibiotics
- Don’t transfuse platelets
Heparin – Induced Thrombocytopenia (HIT)

- common with IV unfractionated hyparin
Type 1 HIT: first 2 day after starting heparin

- direct effect of heparin on platelet NOT immune mediated
- thrombocytopenia is self limited
- no bleeding no thrombosis
Type 2 HIT: 4-10 days after starting heparin

- Etiology: immune mediated allergic reaction against both platelets and heparin.
- Clinical pictures: thromboembolism (DVT, PE, MI,stroke) while pt on heparin
- Diagnosis: clinical finding + thrombocytopenia + HIT antibodies
- Treatment: stop the heparin + direct –acting thrombin inhibitor such as argatroban
or lepirudin.
Warfarin
- Antagonize vit K recycling
- Reduce vit K dependent factor 10,9,7,2 = 1972 in 3-5 days
- Despite its efficacy still has several limitations: interact with other food and drugs,
need to be monitored by INR

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Anticoagulant
Heparin Warfarin
Large anionic, acid polymer Small lipid soluble
Structure
molecule
Route of administration Parentral IV SC Oral
Site of action Blood Liver
Onset of action Rapid Slow
Activates antithrombin which
Mechanism of action decrease action of IIa and Xa Impairs synthesis 1972
Duration of action Acute 60-80 min Chronic 2-3 days

Inhibits coagulation in Yes
No
vitro
Treatment of acute Protamine sulfate
IV vit K and FFP
overdose
Monitoring PTT PT /INR
Crosses palcenta No Yes
H7O
1- H: hemorrhage
2- H: hypersinstivity 1- Hemorrhage
3- H: hypotension 2- Paradoxical
Side effect 4- H: hair loss thrombosis
5- H: hepatic dysfunction 3- Skin ulcer
6- H:HIT syndrome
7- H: hyperK
8- O: osteoporosis

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1- Acute MI 1- A fib
2- DVT 2- L V dysfunction
Usage 3- PE 3- Prosthetic valve
4- DVT
5- PE
New generation anticoagulant

Drug Mechanism Side effect
Dabigatran Direct thrombin inhibitor 1-bleeding
/melagatran 2-GITupset
3-high KFT
Rivaroxaban Direct factor Xa inhibitor 1-bleeding
2-GIT upset
3-high LFT
Antiplatelet
Salicylates Thienopyridines GP IIB/IIIA
inhibitor
Drugs Aspirin Clopidogrel = Plavix Eptifibatide
Ticlopidine = ticlid Tirfiban
Abciximab
Mechanism COX- inhibitor ADP blocker GP IIb/IIIA inhibitor
Side effect -bleeding -bleeding -bleeding
-GIT ulceration -TTP -thrombocytobenia
-impaired renal -neutropenia
perfusion
-metabolic acidosis
Contraindication -active bleeding -active bleeding -active bleeding
-active PUD -active PUD -active PUD
Active bronchial -recent surgery
asthma
-acute renal failure

153

‫‪154‬‬
Chapter 6
Infectious Disease

155

156
INTRODUCTION OF ANTIBIOTICS
Gram positive bacteria: ABCDE + G reat Number of Little Microbes
Leave Many People Seriously Sick
A: Actinomyces B: Bacillus C: Clostridium
D: Diphtheriae E: Enterococcus G: Gardnerella
N: Nocardia L: Lactobacillus M: Mycobacterium
L: Listeria M: Mycoplasma P: Propionibacterium
S: staph S: strept
A. Gram positive cocci

1- semisynthetic penicillinase - resistant penicillin (oxacillin,
cloxacillin, dieloxacillin)
- Treat staphylococcal, streptococcal organisms
- Methicillin is the original drug to this group but not used as cause interstitial
nephritis
- Methicillin- Resistant staphylococcus aureus (MRSA) not respond to this group
- MRSA can be treated by: 1- vancomycin 2- linezolid 3- telavancin 4- daptomycin

5- ceftaroline 6- tigecycline
2- Penicillin G, penicillin vk, ampicillin, amoxicillin
- Penicillin G, penicillin VK >> (natural penicillin) >> streptococci but not treat
staph
- Ampicillin, amoxicillin >> (Broad- spectrum penicillin) >> streptococci +

enterococci + listeria
- Ampicillin >> E.coli
- Only ampicillin + sulbactam Staphylococci
amoxicillin + clavulanate
side effect of penicillin>> is allergy
3- Cephalosporin:
1. 1st generation: cefazolin, cefadroxil, cephalexin >> staph, strept, E.coli, moraxella
2. 2nd generation: cefoxitin, cefoteton, cefuroxime, cefprozil >> as 1st generation
plus:
1- providencia 2- haemophilus 3- klebsiella 4- citrobacter 5-morganella 6-proteus.

157
Allergic cross- reactivity with penicillins

- person allergy to penicillin there is 5- 10 % cross allergy with cephalosporin
- When reaction is rash >> use cephalosporins
- when reaction is anaphylactic + mild infection> Macrolides or Fluoroquinolone
- When reaction is anaphylactic + sever infection >> vancomycin.
4- Macrolides (erythromycin, clarithromycin, azithromycin
5- fluoroquinolones (levofloxacin, gemifloxacin, moxiflacin) ciprofloxacin not

cover strep pneumonia.
6- vancomycin, linezolid, tigecycline, ceftaroline

- Used in life threatening penicillin allergy or MRSA
- linezolid is the only oral
- linezolid, daptomycin, quinupristin cover VRSA
- Ceftaroline is only cephalosporin cover MRSA
- Vancomycin cause red man syndrome, nephrotoxicity
B. Gram- negative Bacilli

1- piperacillin, ticarcillin, mezlocillin (extended spectrum)
- It is anti: pseudomonas
- Cover full range gram negative bacilli
- Cover staph If combined with B-lactamase inhibitor (piperacillin / tazobactam,
ticarcillin/ clavulanate)
2- Cephalosporin:
1- 3rd- generation: ceftazidime, cefotaxime, ceftriaxone, cefotaxime (cover gram
negative)
2- 4th generation: cefepime (broad spectrum for gram positive and negative
- Cover full range of gram negative bacilli
- only ceftazidime + cefepime cover pseudomonas
- 3rd don't cover staph

158
3- Quinolones (ciprofloxacin, levofloxacin,

gemifloxacin, moxifloxacin, ofloxacin
- Cover most enterobacteriaceae: E. coli, proteus,
moraxella, enterobacter, haemophilius, moraxella,
citrobacter, morganella, serratia, klebsiella
- only ciprofloxacin cover pseudomonas
- side effect: affect cartilage, tendon rupture
4- aminoglycosides (gentamicin, tobramycin, amikacin)
- Cover only gram negative
- Side effect: nephrotoxicity, ototoxicity
5- monobactams: only gram negative
6- carbapenems (Imipenem, meropenem, ertapenem, doripenem

- Broad spectrum cover gram negative + positive
- Cover pseudomonas except ertapenem.
- side effect: seizure
C. Anaerobes: covered by:
- Above diaphragm >> clindamycin
- Below diaphragm >> metronidazole
- carbapenems,
-beta lactam / beta lactamase
Notes: Antipseudomonal antibiotics.
2- ceftazidime (only 3rd)
- Cefepime (4th)
- piperacillin / tazobactam, ticarcillin / clavulanic acid
- ciprofloxacin (only Fluoroquinolone)
- carbamens Except ertapenem
- monobactams

159
Classification of antibiotics: according to

1- Mechanism
Inhibit
RNA Inhibit folic acid
Inhibit cell wall Inhibit protein system Inhibit DNA gyrase
polymeras synthesis
e
Macrolides
Pencillins
tetracycline
Cephalosporins Sulfonamides
Aminoglycosides Fluoroquinolones
Carbapenems Rifampin Trimethorprim
Clindamycin Metronidazole
Vancomycin cholaramphenciol
A +T >> 30s
Monobactams
M >> 50s
2- bacteriostatic and bactericidal

160
MENINGITIS
- Infection or inflammation of meninges
Etiology:
1- streptococcus pneumoniae: most common
2- Haemophilus influenza: was the common before vaccine
3- Neisseria meningitides: most common in adult
4- listeria monocytogenes: most common in immunosuppressed
5- Staph aureus: most common in neurosurgery
6- Cryptococcus: more common in HIV
7- RMSF: with ticks
8- lyme, TB, SYPHILIS, VIRUSES
9- group B streptococcus: most common in
neonatal
Clinical pictures:
1- Fever photophobia, headache
2- nuchal rigidity check stiffness, kernig,
brudzinski
3- Nausea, vomiting,
4- Deafness
5- Rash: - petechial rash >> neisseria
-Rash on wrist & ankle with centripetal
spread > RMST
6- Facial nerve palsy + target like erythema >> lyme
disease
Diagnosis:
1- Lumbar puncture: the most accurate test on lumbar puncture is culture CSF but
needs several days so we do CSF analysis
2- Ct scan: before LP in case: Focal lesion, confusion, papilledema.
3- Specific diagnosis:
- Lyme disease: RMST> serology
- Cryptococcus neoforman> India ink test, csf cryptococcal antigen
- Syphilis: VDRL, FTA
- TB: AFB smear, PCR.

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Treatment:
- Vancomycin
- 3rd generation
- ampicillin in case listeria
- dexamethasone: for 4 day and discontinued
if non bacterial
- specific treatment:
1- Staph aureus >> vancomycin
2- lyme disease > ceftriaxone
3- Cryptococcus >> Amphotericin >> fluconazole
4- neurosyphilis >> penicillin IV
5- TB >> 9 - 12 ant tuberculosis
ENCEPHALITIS
-Infection of the brain
Etiology: 1- bacteria 2- protozoal 3- virus (HSV- I) most common cause.
Clinical picture: 1- Fever 2-headache 3-altered mental status 4- Focal
neurologic deficits 5- Neck stiffness
Diagnosis: - CT, MRI: HSV effect TEMPORAL LOBE
- LP -PCR
Treatment:
1- Acyclovir IV > HSV
2- ganciclovier, foscarnet >> CMV
3- Foscarnet >> HSV resistant acyclovir

162
BRAIN ABSCESS
- Collection of infected material within brain parenchyma
Etiology: Ploymicrobial
1- streptococcus 2- Bacteroides 3-
enterobacteriaceae 4- staphylococcus
Clinical picture:
1- Headache 2- Fever 3- focal neurologic
deficits - seizures
Diagnosis:
1- CT scan (initial test)
2- If HIV Pt give pyrimethamin + sulfadiazine. Then repeat ct scan after 10 -14 day
If Respond >> cerebral toxoplasmosis if no response do biopsy
3- If Pt is not HIV do brain biopsy for gram stain + culture
Treatment: 1- Syx (stereotactic aspiration) + 2 medication:
penicillin + metronidazole + 3rd generation
HEAD AND NECK INFECTIONS

1- otitis Media:
- infection of the middle ear between the eustachian tube and the tympanic membrane
Etiology: 1- Strep pneumonia 2- H influenza 3- moraxella catarrhalis
Clinical picture: 1- Ear pain 2 fever 3-decrease hearing
4- physical examination: red, bulging tympanic membrane with loss of light reflex.
5- the most sensitive sign is immobility of
the membrane of insufflations of the ear
with air.
Diagnosis: physical examination 2- no

need for culture.
Treatment:
1- amoxicillin best initial
2- amoxicillin- clavulanate, 2nd generation, 3rd generation
3- Fluoroquinolone but not for children.

163
2- sinusitis:
-infection of the sinuses
- maxillary > 𝑒𝑡ℎ𝑚𝑜𝑖𝑑 > 𝑓𝑟𝑜𝑛𝑡𝑎𝑙 > 𝑠𝑝ℎ𝑒𝑛𝑜𝑖𝑑
Etiology:
- Viral: most common cause
- Bacterial: 1- strep pneumoniae
2- H. influenza 3- M. catarrhalis
Clinical picture:
1- -Facial pain, postnasal drainage (purulent)
2- Headache worse when pt lens forward
3- tooth pain
Diagnosis: 1- Sinus x: ray: not recommended 2- sinus ct scan:
Treatment:
1- Decongestant: oral pseudoephedrine - oxymetazoline spray
2- Oral antibiotics: (same as otitis media)
3- Vial resolve 7-10 days with symptomatic management if not give antibiotics
3-pharyngitis
Etiology: 1- virus (most common) 2- group A- B- hemolytic streptococci (s.

pyogenes) cause
1- rheumatic fever 2- glomerulonephritis
Clinical picture: 1- sore throat 2- cervical adenopathy 3- exudates

covering pharynx
Diagnosis: 1- Rapid streptococcal antigen 2- culture if rapid antigen is negative
Treatment:
1- penicillin main treatment
2- Macrolides, 2nd generation in penicillin allergy

164
4- Influenza:
- Systemic viral illness (influenza A, B)
- Transmitted by droplet nuclei
Clinical pictures:
1- Fever, myalgia, headache, fatigue
2- runny nose (coryza), nonproductive cough, sore throat, conjunctival injection
Diagnosis: 1- Rapid antigen detection methods or swabs. 2- viral culture most

accurate
Treatment:
1- acetaminophen + antitussive
2- neuraminidase inhibitor: oseltamivir, zanamivir should be given with 48 hour of
symptoms.
3- Vaccine recommended annually
LUNG INFECTIONS
1-Bronchitis:
infection of lung limited to bronchial tree
Etiology: Acute exacerbations of COPD
- Acute: 1- viruses 2- M. pneumonia 3- C pneumonia 4- B pertussis
- Chronic: same otitis media - smoking paralyze cilia for 24 hour
Clinical pictures: 1- Fever 2- cough with sputum
Diagnosis: Chest x-ray: Normal
Treatment:
1- mild not treatment resolve spontaneously 2- acute exacerbation: same treatment
of otitis media
2-lung abscess:
- Necrosis of pulmonary parenchyma
Etiology:
1- Anaerobes: peptostreptococcus, prevotella, fusobacterium
2- aerobic: s. aureus, E. coli, klebsiella, pseudomonas
Clinical pictures: 1- Fever, 2- cough with sputum

3- weight loss
4- anemia 5- fatigue
Diagnosis: 1- Xray 2-CT Scan 3- aspiration of

fluid
Treatment: 1- clindamycin. 2- no need for drainage

165
3-Pneumonia:
- infection of lung parenchyma
-Risk factor: smoking, DM, Alcohol, malnutrition, destruction of bronchi,
immunosuppressions.
Etiology:
Clinical presentation:
- Fever,chest pain, cough with sputum, rusty sputum: s. pneumonia
- Like currant Jelly sputum, klebsiella - Hyperventilation
- Physical examination: rales, rhonchi, lung consolidation, dullness to percussion,
bronchial breath sounds, increase vocal fremitus (E >> A)
- Mycoplasma:
1- Dry cough + chest soreness
2- bullous myringitis
3- anemia from hemolysis + cold agglutinin
- Legionella:
1- CNS: confusion, headache lethargy
2- GIT: diarrhea + abdominal pain
- PCP: Dyspnea on exertion - chest soreness With cough - HIV < 200 INL
Diagnosis:
1- chest x-ray: lobar infiltrates, bilateral interstitial
(atypical pneumonia)
2- Sputum culture. Most specific - gram stain
3- Bronchoscopy, thoracentesis, pleural biopsy
4- open biopsy: most specific
5- specific methods:

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- Mycoplasma: serologic Ab titers

- legionllea: specialized culture media, urine antigen
test, fluorescent antibody
- PCP: bronchoalveolar lavage, increase LDH
Treatment: outpatient or hospitalized according to

curb- 65
1- confusion 2- uremia 3-respiratory distress 4- low blood pressure 5- age > 65
-each get 1 point: 0-1 >> out pt 2>> floor 3-5>> ICU
- Hospital acquired pneumonia:

• 5-7 day in hospital
• Gram negative bacilli (pseudomonas, E-coli)
• Gram positive bacilli (MRSA)
• combination:
1- antipseudomonal: ceftazidime/ carbapenems / beta lactam coverage
2- MRSA: vancomycin/ linezolid
3- gram negative coverage: aminoglycosides
-Aspiration pneumonia:
• Aspiration of GI contents in semicomatosed pt (intubation, vomiting of
semicomatosed pt)
• Most common bacteria >> anaerobic (bacteroid, fusobacterium)
• Chest x ray : after 6 hour > infiltration of right lower lobe
• Treatment: clindamycin, lincomycin, metronidazole

167
Pneumococcal vaccine
1- Age < 65 2- chronic: lung, liver, cardiac, renal disease
3- immunocompromised pt: steroids, HIV, splenectomized DM, leukemia, lymphoma
4- Redosing in 5 years. in immunocompromised pt
4-Tuberculosis:
Etiology: - mycobacterium tuberculosis
-Spread by person to person by respiratory droplets
Risk factor: alcoholics, healthcare, worker, prisoners, homeless -

immunocompromised
Clinical pictures: Fever, cough, septum, weight loss, night sweats

- Most common site of primary infection is lung
- most common site of extra pulmonary TB: lymph node
- TB in bone vertebrae: pott's disease
- If spread from lung to other site by blood called milliary TB.
Diagnosis:
1- Chest x-ray(Initial test) apical involvement,
infiltrates, cavitations, adenopathy, effusion,
calcified nodal (ghon complex)
2- sputum staining with acid-fact bacilli.
3- culture (specific) need 4-6 week
4- thoracentesis, gastric aspirate, biopsy, needle
aspiration
- PPD is not diagnostic.
Treatment: 4 drugs for 2 month then 2drug for 4month
INH >> 4 month
2 month RIF >> 4 month
PZA
ETB
Give vit B6 (pyridoxine) with INH to prevent peripheral neuropathy
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- Don't give PZA or streptomycin for pregnant

- Give steroid for TB meningitis or pericarditis
side effects
- All TB drugs cause hepatotoxicity except streptomycin
- INH > peripheral neuropathy.
- Rifampin >> orange / red color of all body fluids
- Ethambutol > eye optic neuritis.
- Pyrazinamide >> hyperuricemia
Treatment of latent TB infection. - Latent TB: is asymptomatic non infection pt but
maybe active in future.
- PPD and IGRA is used for screening in asymptomatic population at risk of TB
- PPD is done by injection of purified protein derivatives of TB intradermally then
measures the induration after 48- 72 hour (not the erythema)
consider positive If the following:
≥5 mm:
• Close contacts of active TB cases
• HIV-positive persons
• Abnormal chest x-ray consistent with old, healed TB
• Steroid use or organ transplantation recipients
≥10 mm: High-risk groups,
• healthcare workers, prisoners, nursing home residents;
• recent immigrants (within 5 years) from areas with a high prevalence; homeless
patients;
• persons with immunocompromise, such as those with leukemia, lymphoma,
diabetics, dialysis patients, and injection drug users who are HIV-negative whose
HIV status is unknown;
• children <4 years of age,
• infants, children, and adolescents exposed to adults at high risk of TB.
≥15 mm: Low-risk populations, i.e., not the people described above, i.e., people who
should never have been tested in the first place.
- If the PPD positive do chest x-ray if abnormal do 3 sputum AFB stain if positive
start 4 drug therapy.
- If the PPD positive with x-ray finding give INH/B6 for 9 month

169
causes of hemoptysis :
1-bronchitis: most common cause 2-lung CA 3-TB
4-bronchoectesis 5-CF 6-churg-struss 7-PE
8-viral pneumonia 9-LVF 10-good pasture
11-pulmonery hemosiderosis

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ACUTE VIRAL HEPATIC INFECTIONS:

- Viral hepatitis is an infection of liver caused by hepatitis A, B, C, D, and E
− Drug- induced hepatitis (isoniazid -

alcohol) present with same
symptoms.
− HBV, HCV > serum sickness (Joint
pain, Rash vasculities,
glomerulonephritis.
− HBV, HCV> cryoglobulinemia
− HBV > Polyarteritis nodosa.
− HEV > Pregnant.
Diagnosis:

171
- High total & direct bilirubin

- High AST, ALT (ALT higher)
- Drug & alcohol - induced hepatitis
(AST higher)
- Abnormal prothrombin time,
albumin
- Hepatitis A, C, D, E, IgM>>
Acute infection
- Hepatitis A, C, D, E IgG >> Old
infection
- Hepatitis activity Followed by
PCR-RNA viral load(not for
diagnosis)
- Hepatitis B surface antigen >>
diagnosis
- HBVE antigen + IgM core Ab>
acute
- Loss of surface Ag + high
hepatitis surface Ab> Resolution
-HBVc IgG + HBVE Ab only
marker in window period (2-6 week)
Treatment:
- Acute HBV = no treatment.
- Chronic HBV: Interferon, entecavir, adefovir or lamivudine
- HCV: sofosbuvir/ledipasvir (Harvoni), simeprevir (Olysio), sofosbuvir (Sovaldi)
and Viekira Pak (ombitasvir, paritaprevir and ritonavir tablets co-packaged with
dasabuvir tablets that may be prescribed with or without ribavirin)
-while treatment HCV the virus is undetectable within 4-12 weeks and will remain
through treatment
- pt is cured from HCV when sustained virologic response achieved or continuation of
his undectable status 12-24 weeks after therapy
Needle stick from HBV surface Ag positive PT

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- If not protective pt: HBIg+ HBV vaccine

- If protective >> no further therapy.
- no postexposure prophylaxis to HCV
Drug induce hepatitis :

1- alcohol : AST > ALT ( most common cause )
2- paracetamol
3- ASA
4- tetracyclines
5- sulfonamides
6- anti- TB
7- anti-epilepsy
8- amidarone
9- methyldopa
10- propylthiouracil
11- statin
GENITAL AND SEXUALLY TRANSMITTED

INFECTIONS
Urethritis:
Etiology:
1- Gonococcal urethritis: Neisseria gonorrhea
2- Nongonococcal urethritis: chlamydia trachomatis, ureaplasma urealyicum,
mycoplasma hominis, trichomonas, herpes simplex
Clinical pictures:
1- Purulent urethral discharge
2- Dysuria
3- Urgency
4- Frequency

173
Diagnosis:
- Gonorrhoeae: smear >> gram negative,coffee bean –shaped diplococcic
intracellularly
- Culture is most accurate
- Chlamydia: serology for swab of urethra or ligase chain reaction for urine
Treatment:
- Ceftriaxone, cefixime: IM single dose
- Azithromycin: orally single dose
- Doxycycline for 7 days
Syphilis:
Etiology: treponema pallidum.
Clinical picture:
1- congenital:
- early: symptomatic up to age 2
- late: symptomatic, Hutchinson teeth, scar & interstitial keratitis, bony
abnormalities (saber shin)
2- Acquired:
I - primary stage:
- Chancre appear within 3rd week disappear 10 - 40 day.
-painless, rubbery, discrete, regional lymphadenopathy

- Chancre appears on penis, anus, rectum, and cervix.
II - Secondary stage:
- Cutaneous rash (6- 12 weeks): pinkish or pale red in
white pigmented spot - copper colored macules in
black
- Lymphadenopathy > condylomata late ً ‫معدية جدا‬
III- latent stage:

- Asymptomatic: May persist for life
IV- Tertiary syphilis:

- 3-20 year after primary infection
174
- Gumma (chronic granuloma) > heals with scar

- Not contagious.
- May appear as cardivoscalar or neurosyphilis
- Argyll Robertson pupil > small, irregular pupil reacts normally to accommodation
but not to light.
- Tabes dorsalis: pain, ataxia, sensory changes, loss of tendon reflex
Diagnosis:
- Screening test: VDRL, RPR
- Specific test: FTA - ABS - MHA- TP- Drake field exam of chancre
Note: False positive of VDRL:
EBV, collagen vascular disease, TB, subacute bacterial endocarditis
Treatment:
- Primary or secondary > 2.4 million benzathine penicillin IM / week for 1 week.
- Latent > 2.4 million benzathine penicillin Im / week for 3 week
- tertiary > 10-20 million units penicillin Iv for 10 day
- In case of penicillin allergy > doxycycline
Note: jarisch herxheimer reaction occurs 6-12 hour from initial treatment (malaise,
fever, headache, sweating, exacerbation & lesions.
Genital Herpes:
Etiology: herpes virus type 2
- Virus can be transmitted in asymptomatic phase while shedding the virus
Clinical pictures:
1- Itching and soreness first symptoms
2- Vesicles on skin or mucous membrane become
eroded and painful with circular ulcer and red
areola
3- Ulcer are scarring
4- Inguinal lymphadenopathy
Diagnosis: Tzanck test and culture
Treatment:
- Oral acyclovir famciclovir or valacyclovir
- Explain to pt that disease may relapse
- Chronic suppressive therapy for frequent recurrence
175
Genital Warts: (condylomata acuminate / venereal warts)

Etiology: papilloma virus
Clinical pictures:
- Soft, moist, minute,pink or red swelling
- Rapidly growing and become pedunculated
- Cauliflower appearance
Diagnosis: clinical appearance
Treatment:
1- Destruction (curettage, sclerotherapy, trichloroacetic
acid)
2- Cryotherapy
3- Podophyllin
4- Imiquimod
5- Laser removal
URINARY TRACT INFECTIONS (UTI)

1- Cystitis: Infection of bladder.
Etiology: E. coli (most common), proteus, klebsiella,
Risk Factor:
1- Tumor, stones, strictures, BPH, neuralgic bladder
2- Sexual intercourse (honey moon cystitis)
3- Catheters (3-5 % per day)
Clinical picture:
1- Dysuria, Frequency, urgency
2- suprapubic Pain not Flank
Diagnosis:
1- urine analysis: WBCS, RBCS, bacteria,Nitrates (gram negative infection) (initial)
2- Urine culture. > 100,000 colonies of bacteria per ML. (conformation)
Treatment:

176
- TMP/ SM, nitrofurantoin, quinolone > 3 day - Dm pt > 7 day
2- Acute Bacterial Pyelonephritis:

Etiology: Same cystitis
Risk factor:same cystitis
Clinical picture:
1- Chills, fever
2- flank pain, costovertebral tenderness
3- nausea vomiting
4- frequency, Dysuria
Diagnosis: clean catch of urine
- Culture, sensitivity: > 100,000 bacteria /ml
Treatment:
- Fluoroquinolone, TMP/SMZ, 3rd generation 10-14 day

- not improve within 48-72 hour > CT scan, U/S
3- Perinephric abscess
- Collection of infected material around the kidney within gerota fascia
Etiology: same cystitis.
Risk factor: same cystitis.
Clinical pictures:
1- Fever
2- Flank pain. palpable mass
3- Persistence of Pyelonephritis like symptoms, despite treatment
Diagnosis:
1- Urinalysis + culture.
2- ULS
3- CT, MRI
4- aspiration of the abscess
Treatment: Ab + drainage.
- Ab: 3rd generation / ticarcillin/ clavulanate (antipseudomonal) +aminoglycoside

177
BONE & JOINT INFECTIONS
1- Osteomyelitis:
-Infection of bone including marrow,cortex, periosteum.
Etiology: (staphylococcus aureus)
Child > tibia, femur.
Adult > vertebral bodies (lumbar)
Clinical pictures:
- Pain, erythema, swelling, tenderness.
- Ulceration > draining sinus tract
Diagnosis:
1- plain x: ray: initial test

2- ESR: follow up treatment
3- Bone biopsy- culture: best diagnostic.
4- Ct scan, indium gallium
5- MRI, technetium bone scan: early
detection
Treatment:
- Adult > syx + Ab.
- Children > Ab.
- Syx = wound drainage, debridement, removal infected hardware
- Ab: semisynthetic penicillin or vancomycin
Plus
Aminoglycosides or 3rd generation

178
2- Septic arthritis:
Infection of joint.
Etiology:
- Gonococcal (neisseria gonorrhoeae) most common >
sexual active
- Nongonococcal (staph, strep, viruses, spirochetes) >
Hematogenous, bites, trauma, RA, OA, IV users..
most commonly gram positive
Clinical picture:
- Nongonococcal: monoarticular, swollen, tender
erythematous joint, decrease Joint motion, most common knee
- Gonococcal: migratory polyarthralgia,tenosynovitis, skin (petechiae purpura).
Diagnosis:
- Nongoncoccal: Joint aspiration + gram stain >> PMN > 50,000 + gram positive +
low glucose
- Gonococcal: culture of other sites: cervix, rectum, pharynx, urethra
Treatment: Joint aspiration + Ab
- Nongonococcal: nafcillin, oxacillin, vancomycin + 3rd generation or
aminoglycoside
- Gonococcal:ceftriaxone.
3-Gas gangrene:
- necrotizing destruction of muscle by gas producing organism.
Etiology: wound contamination with clostridium perfringens without exit to surface.
Clinical pictures:
- Start 1-4 day: pain, swelling, edema
- later: hypotension, tachycardia, Fever, crepitation over wound
Diagnosis:
1- Gram stain: positive rods.
2- Culture.
3- x-ray gas bubbles
4- Direct visualization >> pale, dead,
brownish muscle with sweet smelling
discharge >> diagnostic
Treatment:
1- Penicillin 24 million/day or clindamycin
2- Surgical debridement.
3- Hyperbaric o2

179
CARDITIS
1-Infective endocarditis:
Colonization of heart valves with microbial

organisms causing friable infected vegetations &
valve injury.
- Aortic & mitral valve most commonly affected.

(M > A > T > P )
Etiology:
- Native valves >> strep viridans

- Narcotic addicts >> staph aureus
- Prosthetic valves >>acute (first 2 month): staph epidermidis.
Later: strep viridians
- Colon cancer: strept bovis
Acute infective Subacute infective endocarditis
endocarditis
Mcc S.aureus Strept viridans
Valve Normal valve Abnormal valve
Vegetation Large bulk, on arterial Small, composed of: Fibrin
side platelets - debris, bacteria
Risk Factor Iv drug users. VSD, stenosis, prosthetic valves,

indwelling cath, MVP, marfan,
bicuspid aortic
Clinical course 1- rapid onset fever, 1- Slow onset of vague symptoms.
sepsis 2- Malaise, low grad fever.
2- splenomegaly 3- Weight loss, flue like sym.
3- abscess, valve 4-Destruction valve
destruction embolic 5-less fatal
complication

180
Clinical picture:
Complications:
1- Congestive heart Failure (most common cause of death)

2- Septic embolization brain, kidney, spleen, coronary
3- Glomerulonephritis with nephritic syndrome or renal failure

181
Diagnosis: duke criteria.
Possible diagnosis
Definitive diagnosis
1 major + 1 minor
2 major
OR
OR
3 minor
1 major + 3 minor
OR
5 minor
Treatment:
Empiric treatment: vancomycin+ gentamicin then change when culture result
- Strept viridans >> penicillin
- Staph aureus >>nafcillin
- MRSA >> Vancomycin.
- Enterococcal >> penicillin + gentamicin
Indication of syx:
Major criteria
• Congestive heart failure, progressive or unresponsive to “simple” measures
• Recurrent systemic emboli
• Persistent bacteremia despite adequate antibiotic therapy
• Fungal etiology
• Extravalvular infection (atrioventricular block, purulent pericarditis)
182
• Prosthetic valve dehiscence or obstruction

• Recurrence of infection despite adequate therapy
Minor criteria
• Congestive heart failure resolved with medical therapy
• Single systemic embolic event
• Large aortic or mitral vegetations on echocardiography
• Premature mitral valve closure in acute aortic insufficiency
• Prosthetic valve infection due to organisms other than highly penicillin-
sensitivestreptococci
• Tricuspid endocarditis due to Gram-negative bacilli
• Persistent fever without other identifiable cause
• New regurgitation in an aortic prosthesis
. Prevention of bacterial endocarditis:

- Prosthetic valve
- Unrepaired cyanotic heart disease
- Pervious endocarditis
- Transplant status
- HOMC , Rheumatic fever + dental, skin , respiratory, GIT,
muscle-skeltal procedures
- IVDU
- DM , HIV
- hemodylasis
- poor dentation
>> Give amoxicillin , ampicillin ( clindamycin , macrolides if pencillin allergy ) 30-

60 min before dental or respiratory surgery
>>Give cephalexin ( clindamycin if pencillin allergy ) 30-60 min before skin or soft
tissue surgery

183
Causes of clubbing :
1- Lung: lung CA, inters titial lung disease, sarcoidosis, fibrosis, TB,
lung abscess, empyem a,bronchiectasis,cyctic fibtosis,
mesothelioma
2- Heart: congential cyanotic heart disease, TF4, TGA, endocarditis,
atrial myoxoma
3- GIT: malabsorption, crohns,
UC, liver cirrhosis
4- Hyperthyroidism
5- Familial and racial cl ubbing
(pseudo-clubbing)
- Note: asthma and COPD
don't cause clubbing
- Clubbing test with
Schamroth's window test
2-Myocarditis:
Infection of heart Muscle.
Etiology:
1- Viruses coxsackie B: (Most common cause)

2- Bacteria: rickettsia,parasite.
3- Non-infection: Radiation, drugs, collagen disease, hyperthyroidism.
Clinical pictures:
1- Dyspnea + Fatigue (most common symptoms)

2- May asymptomatic >> chest pain, arrhythmia, death
3- S-3 gallop + murmur
Diagnosis:
1- ECG: - Nonspecific ST-T wave.

- Heart block.
2- high Cardiac enzyme (CK - MB, troponin)
3- Echo: left ventricular dysfunction
4- Viruses isolation from stool, saliva
5- Serum titer Ab
6- Endomyocardial biopsy (most specific)
Treatment: Supportive for viral until resolving spontaneously

184
LYME DISEASE (low yield)

Etiology: bite of Ixodes scapularis tick which transmits borrelia burgdorferi
Clinical picture:
- Symptoms begin 3-30 day after bite tick
- Erythema migrans rash (bulls eye)
- Flue like illness fever, chills, myalgias
- Neuro: 7th nerve palsy, meningitis, encephalitis
- CVS: AV block, Myocarditis, pericarditis-
arrhythmia
- Joint: migratory polyarteritis
Diagnosis:
- -Rash + one late manifestation + Lab

- Lab test: ELISA + Western blot
- Treatment on presence of Rash
Treatment:
- Minor symptoms: doxycycline or amoxicillin

- cardiac or neurotic manifestation: IV ceftriaxone
Immune system
Immune System is dived for 2 subsystems:
1) Innate system (First line) include:

I- Surface barriers: mechanical, chemical, biological
-Mechanical skin, Coughing, sneezing, mucus.
-Chemical lysozyme, phospholibase A2, proteases
-Biological GIT + vaginal bacterial flora.
II- Inflammation: redness, swelling, heat, pain produced by:
1- eicosanoids: like:
• Prostaglandin (fever, dilatations blood vessels)
• Leukotrienes: attract WBC’s
2- Cytokines:

185
• interleukins: communication between WBC’s

• Chemokins: chemotaxis
• Interferon: antiviral
• TNF
III- complement system: group of protein that attached to surface of bacteria to help
antibodies (C1-C9)
• C2 deficiency is the most common complement defect
• C1 deficiency can produce angioedema
• C1-C4 deficiency increase risk of encapsulated bacterial infection:streptococcus
pneumonia (pneumococcus), haemophilus influenzae (HIB), neisseria meningitis
(meningeococcus)
• C5-C9 deficiency increase risk of neisseria infection (meningeococcus+
gonococcus (neisseria gonorrhea)
IV- cellular barriers:
- Phagocytes (macrophages in tissue, neutrophils in blood, dendritic cell (antigen
presenting cell to T cell).
- mast cell, basophile
- Eosinophills
- Natural killer cells: destroy tumor cell, virus infected cell.
2) adaptive immune system: (lymphocyte) 2 types:
1- T- cells (cell mediated Immunity) include:
- Killer T cells (CD8)
- Helper T cell (CD4)
2- B- cell (humoral immunity (CD20) (CD19)
-Converted into plasma cell that produces ( Ig MAGED)
• IgM >>the largest Ig & the first Ig produced in infection
• Ig A >> found in secretion: mucous, saliva, tear, milk.
• Ig G >>the smallest Ig (can cross placenta) produced after IgM & remain in
blood as memory for old infection.
• IgE >> for allergy + parasite
• IgD >> activates basophils + mast cells.

186
ACQUIRED IMMUNE DEFICIENCY SYNDROME
Etiology: human immunodeficiency virus (HIV)
- retrovirus RNA virus

- Attack CD4 T cell (helper)
- It needs 10 year to appear symptoms because
HIV kills 50-100 cells / ml/year of CD4 which
takes 5-10 years to Drop CD4 from 700 / mm3
>>200/mm3
- Transmitted by sexual intercourse + drug
injections.
Opportunistic infection in AIDS
1. Pneumocystis jirovecii (carinii) (CD4 < 200/ml)

- Clinical picture: pneumonia: Dyspnea, dry cough, fever, chest pain
- Diagnosis: - bronchoscopy with bronchoalveolar lavage
-Chest x ray bilateral, interstitial infiltrates
-High LDH
Treatment:
1. TMP – SMZ. (first line) >>rash

2. Pentamidine: pancreatitis, hyperglycemia, hypoglycemia
3. Steroids: used in serve pneumonia paO2<70 mm/ mg or Aa > 35.
Prophylaxis: TMP/ SMZ most effective
2. Cytomegalovirus (CD4 <50/ml).
Clinical pictures:
1. Retinitis: blurry vision, double vision
2. Colitis: diarrhea
3. Esophagitis: odynophagia, fever, chest pain (endoscopy >> multiple shallow
ulcer in distal esophagus).
4. Encephalitis: altered mental status, cranial nerve deficits.
187
Diagnosis:
1- Fundus Exam = Retinitis

2- Colonoscopy with biopsy = diarrhea
3- Upper endoscopy with biopsy for ulcer
Treatment:
1- Oral valganciclovir- retinitis or GIT CMV

2- IV ganciclovier= CNS CMV or not tolerate oral medication (netropnia)
3- Cidofovir: failure ganciclovier (Renal toxicity).
3. Mycobacterium avium complex (CD4 < 50/ml)
Clinical pictures: fever, night sweats anemia, diarrhea
Diagnosis:
1- Blood culture
2- Culture of bone marrow liver
Treatment : clarithromycin + ethambutol + rifabutin
Prophylaxis:
- azithromycin orally once week.

- clarithromycin twice week.
4. toxoplasmosis (CD4 <100 /ml)
Clinical picture: Brain mass,headache, confusion, seizures, focal neurologic deficits
Diagnosis: CT, MRT >> ring enhancing lesion
- give 2 week pyri / sulfadiazine if shrinkage it diagnostic if not do brain biopsy.
Treatment: pyrimethamin + sulfadiazine + folic acid
prophylaxis: TMP/ SMZ or Dapsone.
5. Cryptococcosis (CD 4< 100/ ml)
Clinical pictures: meningitis, fever, headache, malaise
Diagnosis:
- LP - serum cryptococcal antigen test

188
Treatment: Amphotericin 10-14 day >>fluconazole.
Vaccinations:
HIV Pt should receive: pneumococcus, influenzae, HBV, varicella
Monitoring the Immune system:
1) CD4 cell count: help in:
- determine the risk of opportunistic infection.

- when to start prophylactic
- when to start antiretroviral (<500)
- Adequacy of response to antiretroviral.
2) Viral load monitoring
- To determine adequate response to therapy

- When initial antiretroviral (55.000 – 100.000)
Antiretroviral therapy
1- Nucleoside Reverse Transcriptase Inhibitors
• Zidovudine (ZDV or AZT) >>Leukopenia, anemia, gastrointestinal
• Didanosine (DDI)>>Pancreatitis, peripheral neuropathy
• Stavudine (D4T) >>Peripheral neuropathy
• Lamivudine (3TC) >>Nothing additional to placebo
• Emtricitabine>>Structurally related to lamivudine; few side effects as for

lamivudine
• Tenofovir is a nucleotide analog as compared to the others that are nucleoside

analogs.
• Abacavir >>Most important side effect is a hypersensitivity reaction that usually

occurs in the first 6 weeks of therapy. Patients may have a rash, fever,
nausea/vomiting, muscle and joint aches, and shortness of breath. In these cases, the
drug should be immediately stopped and never restarted because recurrence of
hyperactivity symptoms can be rapid and life-threatening.
• Zalcitabine (DDC)>>Pancreatitis, peripheral neuropathy, lactic acidosis

189
2- Protease Inhibitors. Hyperlipidemia, hyperglycemia, and elevated liver enzymes

for all in the group; abnormal fat loss (lipoatrophy) from the face and extremities with
redistribution of fat in the back of the neck and abdominal viscera can be seen.
• Nelfinavir>>Gastrointestinal
• Indinavir >>Nephrolithiasis (4%), hyperbilirubinemia (10%)
• Ritonavir >>Severe gastrointestinal disturbance
• Saquinavir>>Gastrointestinal
• Amprenavir
• Lopinavir/Ritonavir combination >>Diarrhea
• Atazanavir>>Diarrhea, asymptomatic hyperbilirubinemia
3- Non-Nucleoside Reverse Transcriptase Inhibitors. These drugs are

noncompetitive inhibitors of reverse transcriptase.
• Efavirenz >>Neurologic; somnolence, confusion
• Nevirapine>>Rash, hepatotoxicity
• Delavirdine >>Rash
• Rilpivirine
When to start therapy?
• Once diagnosed regardless CD4 count
What to start: On the following
• 2 nucleosides + protease inhibitor

• 2 nucleosides + Efavirenz
• Emtricitabine+ Tenofovir+ Efavirenz available as (1) pill
What is considered adequate therapy?
- Drop at least 50% of viral load in first month
Pregnant patients:
- all children of HIV mother will carry maternal Ab so will be positive by ELISA
- Only 25-30% will remain truly infected
- Pregnant with serious disease treated by triple antiretroviral as non pregnant
- C- section only for uncontrolled
- Only Efavirenz is teratogen

190
Note: Breast Feeding transmit virus to infant
postexposure prophylaxis (Needle stick injury)
Zidovudine + lamivudine + Nelfinavir >> 4 week
Tetanus
etiology:
- clostridium tetani >> take 1-7 day to develop spore
clinical picture:
- Tonic spasm of voluntary muscle, respiratory arrest, dysphagia, irritability, neck
stiffness, lock jaw flexion of arms + extension of lower limb
Treatment (prophylactic)
- T dap every 10 years
- Immediate debride wound.
- Antitoxin, ATS
- Penicillin 10-14 day

191
Brucellosis:
Etiology: brucella melitsis, abortus, suis,canis
- infection caused by ingestion of milk from infected animal
Clinical picture:
- Malaise, headache, weakness, night sweats, lymphadenopathy,

hepatsplenomegaly, arthritis, orchitis, meningitis, endocarditis.
Diagnosis:
1) Leukopenia, anemia
2) Serum agglutination test (most common)
3) Blood culture
4) CSF culture
Treatment:doxycycline + Rifampin >>6 week
Preventation: hygiene + pasteurization of milk

192
Typhoid fever
Etiology: salmonella typhi
- Transmitted by Feco- oral transmition
Clinical picture: (4 stages)
1- Stage (1) >> (1st week):

- fever fluctuations Bradycardia, malaise, headache
- Leukopenia, positive blood culture, widal test negative
2- stage (2) >> (2nd week):

- high fever (40c), Bradycardia, rose spots (chest + abdomen), diarrhea, constipation,
- positive widal test.
3- Stage (3) >> (3rd week):

- encephalitis, abscesses, cholecystitis, endocarditis, osteitis.
- Intestinal hemorrhage: bleeding in congested peyer’s patches.
- Intestinal perforation (ileum)
4- Stage (4) >>(4th week) resolving fever
Diagnosis:
- Culture (1st week) blood, stool,

bone marrow
- Widal test (2nd week) =
salmonella Ab
Treatment:
- Ciprofloxacin
(Fluoroquinolone) for 14 day
- Chloramphenicol but has side effect (Aplastic anemia, Gray baby syndrome)
Cholera
Etiology: Vibrio cholera
- Transmitted by infected drinking water, shellfish and food contaminated by flies

or hands of carriers

193
Clinical pictures:
1- Painless watery diarrhea (rice water diarrhea)

2- Vomiting
3- Dehydration
Diagnosis:
1- Stool dark filed microscopy: shooting star motility of V.cholera

2- Culture
Treatment:
- oral rehydration solution

- IV fluid and electrolyte replacement \
- Tetracycline or ciprofloxacin
Preventation:
1- Strict personal hygiene

2- Clean piped water
3- Good food hygiene

194
Chapter 7
Nephrology

195
‫‪Chapter 7 : Nephrology‬‬

‫‪196‬‬
Anatomy of kidney
- kidney receive 20-25% of cardic output
- it is retroperitoneal organ (T12 – L3)
- GFR: glomerular filtration rate =125 ml/min
- nephron is the function unite of kidney
- parts of nepron and function :
I- glomerulus >> ultrafiltration 180 L / day
II- proximal convulated tubule >>

1- reabsorption of glucose, H2O, NaCl, HCO3
2- secretion of H+
III- loop of henle >> reabsorption of H2O, NaCl, K
IV- Distal convoluted tubule >>

1- has aldosterone receptor
2- reabsorption of NaCl, Ca, H2O, HCO3
3- secretion :H+, K+, Ca
V- connectin tubule :
1- has ADH receptor
2- reabsorption of NaCl, H2O, K+, HCO3
3- secretion of urea , ammonia

197
ACUTE RENAL FAILURE

Definition:
rapid rise in BUN or Cr over period of several hours to days.
- Azotemia= Renal insufficiency: means buildup of azole groups or nitrogen in the

blood >>don’t need dialysis.
- Uremia= sever renal failure = urea in the blood= >>need dialysis.
Clinical picture:
- Acidosis, mental status changes, Hyperkalemia, fluid overload, anemia,

hypocalcemia, pericarditis, bleeding diathesis.
Classification:
1. Prerenal azotemia: decrease perfusion to the kidney.

2. Intrarenal: Kidney defect = tubular or glomerular.
3. Post renal: decrease drainage from the kidney
Diagnosis:
1) BuN:
- False positive: blood in guts, big protein meal
- False negative:liver disease, malnutrition, SIAD
2) Creatinine: metabolic product of skeletal muscle.

198
Prerenal Azotemia:
Causes:
1) Hypovolemia (dehydration, burns, poor oral intake, vomiting diarrhea, sweating,

hemorrhage.
2) Hypotension shock.
3) Third spacing of fluids: peritonitis- diuresis- low aldosterone.
4) Decrease cardiac output: (HF, pericarditis, coarctation of aorta.)
Diagnosis:
1) BUN: Cr = 20: 1
2) Low Una
3) Low fractional excretion of Na.
4) High urine osmolality (> 500).
5) High urine specific gravity (>1.010)
1- Renal artery stenosis:
1. Atherosclerosis 2. Fibromuscular dysplasia
2- Hepatorenal syndrome:
- Hepatic Failure >> intense vasoconstriction of afferent arteriole >> decrease renal
perfusion.
- No improvement in renal failure after 1.5L of colloid like albumin is diagnostic.
- Treatment
• liver disease
• Midodrine: (alpha agonist), octereoide
• Liver transplantation.
3- ACE inhibitor on the kidney:
- Angiotension has vasoconstrictive effect on efferent
- ACE inhibitor has vasodilatation on efferent this lead to decrease KFT and rise BUN
and Cr but the overall effect on kidney decrease intraglomerular hypertension
which decreasing proteinuria and the rate of progression of renal failure (especially
in DM pt).

199
Postrenal Azotemia:
Causes:
1. Stone or clot in bladder.

2. Bladder cancer.
3. Prostate hypertrophy or cancer.
4. Bilateral ureteral disease.
5. Neurogenic bladder.
Diagnosis:
1. BUN: Cr = 20:1 >>10:1

2. Low Urinary Na.
3. Low fractional excretion of Na.
4. Distended bladder.
5. Bilateral hydronephrosis on U/S or CT
6. Large residual volume >50 ml.
Tubulointerstitial Disease:
1- Acute tabular disease.
- Ischemia for tubule from other cause (Hypotension).
Three phases:
1) Prodromal time between injury and renal failure.

2) Oliguric < 400ml/24 hour or anuric < 100ml/ 24 hour.
3) Postoliguric. Diuretics phase.
Diagnosis: normal urine output :

-adult =0.5-1 ml/kg/hr
1- BUN: Cr = 10:1 -children = 1-1.5 ml/kg/hr
-infant = 1.5 -2 ml/kg/hr
2- High Urinary Na
3- High Fractional excretion of Na. oliguria
4- Low Urine Osmalality < 350 urine output <0.5 ml/kg/hr
urine output <400 ml/day
Treatment:
anuria :
1) Treat the cause. urine output < 100- 50 ml/day
2) Hydration.
3) Supportive care.
2- Allergic interstitial nephritis:

200
Etiology:
1. penicillins, cephalosporins, allopurinol, Rifampin, Quinolones, sulfa drug

(thiazides, furosemide, acetazolamide,
- Can occur from 1st does:
2. Infection: CMV, rickettsia, strept.
3. Autoimmune disease: SLE, sJogren syn
Clinical picture:
- Fever - rash - Joint pain
Diagnosis:
1) Esinophilia + high IgE

2) Eosinophiluria, hematuria, proteinuria (urine analysis)
3) Hansel stain or wright stain for urine = Eosinophiluria
4) Kidney biopsy (most accurate)
Treatment:
- Stop offending drug.

- Short course of steroids
3- Pigments (hemoglobin / Myoglobin)
Etiology:
1) Rhabdomyolysis: (release, myoglobin from muscle) causes by. Crush injury,

seizures, sever exertion (marathon), hypok, hypopho4, medication (statin).
2) ABO incompatibility (release hemoglobin).
Diagnosis:
1) ECG, or K level: most important

2) Urine analysis, (initial) but can't distinguish between hemoglobin, Myoglobin,
RBC.
3) CPK (confirmation) > 10.000 – 100.000
4) Acidosis + low HCOS
5) Hyperphosphatemia, hypocalcemia, hyperuricemia.
6) BUN: Cr = 10: 1 + high urine Na, high frac EX Na…

201
Treatment:
1) If ECG abnormal (peaked Twave)= calcium chloride

2) Hydration + mannitol.
3) Alkalinizing of urine with HCO3
4-protins
- Bence – joes prteins. (Myeloma)
5- Crystals:
I- oxalate – antifreeze ingestion in suicidal pt
>>metabolic acidosis with high anion gap
treatment fomepizde – dialysis - Na HCO3-
I- Urate: tumor lysis syndrome:
Treatment: Allopurinol with alkalinization of urine.
6-Hypercalcemia
- Ca can precipitates in kidney tubule >>stones

- the most common cause is hyperparathyroidism
7-Toxins:
- NSIAD, Aminoglycosides cephalosporins, contrast agent, Amphotericin,
chemotherapy, heavy metal
- Need 3-5 day to cause the effect.
- no rash, joint pain, fever.
1- Aminoglycoside Tobramycin least nephrotoxic
2- Amphotericin B >> low Mg, HCO3-, K.
3- Atheroembolic disease.
- Pt undergoes vascular catheter, procedure >> renal failure several day later.
Clinical picture:
- Eosinophilia, low complement, bluish
discoloration of fingers.
- Livedo reticularis
diagnosis: skin biopsy show cholesterol

crystals in skin

202
Treatment: no therapy but high dose statin can try.
4-Contrast agent:
- Renal failure 12- 24 hour after the agent

- Cause intense vasospasm of afferent arteriole because its hypertonicity.
5-Other toxins: Pentamidine, vancomycin, cyclosporine lithium, Indinavir.
8- Analgesic nephropathy, cause renal failure by several mechanisms:

1. Interstitial nephritis.
2. Direct toxic effect on tubules.
3. papillary necrosis
4. Inhibition of vasodilator prostaglandin in the afferent
5. Membranous glomerulonephritis.
9-Papillar necrosis:
- Sickle cell disease, DM, Urinary obstruction, chronic Pyelonephritis + ingestion

of NSAID.
Clinical picture: sudden onset of
1. Flank pain 2. Hematuria 3. Pyuria 4. Fever.
Diagnosis:
1. Urine analysis: WBc’s RBc’s

2. No grow organisms on culture.
3. CT scan: most accurate
Treatment: no specific therapy.
Prevention of contrast – induced renal failure:
- 1-2 liters of N/S over 12 hour before procedure

- HCO3-
- N- acetyl cysteine

203
GLOMERULONEPHRITIS (Nephritic syndrome)

- Inflammation of the glomerulus on the basis of an autoimmune event, circulating
antibodies vasculitis.
Etiology:
Clinical picture:
1) Edema: first in periorbital area or scrotum

2) Hematuria
3) Red cell cast
4) HTN
5) Proteinuria < 2 gram / 24 hour
Diagnosis:
- Blood test: ANCA, basement membrane Ab,

ANA, antistreptolysin
- Renal biopsy most important
Treatment: specific to the cause
1) Wegner granulomatosis:
- Systemic vasculitis involves: kidney, lung, upper respiratory tract.
Clinical pictures:
- Chronic upper and lower respiratory illness not responding to AB.
- Renal disease.
- Involvement of skin, joint, eye GII, neuropathy

204
Diagnosis:
- ESR, anemia, Leukocytosis
- C- ANCA initial test
- Biopsy of kidney, nasal septum, lung >>
accurate
Treatment: cyclophosphamide and steroids:
2) Churg – strauss syndrome

- same wegner + asthma + eosinophilia + other
atopic disease
diagnosis:
- High eosinophil
- P- ANCA
- Lung biopsy most accurate
Treatment: glucocorticolds and cyclophosphamide
3) Good pasture syndrome:

- Idiopathic disease of lung and kidney only
Clinical picture:
- Kidney >> Hematuria and proteinuria.
- Lung >> hemoptysis, cough, SOB.
Diagnosis:
- Antibasment membrane Ab to type IV collagen.
- Lung or kidney biopsy
Treatment: plasmapheresis and steroids
4) Polyarteritis nodosa:
- Small and medium vasculitis affects every organ except the LUNG.
- Involvement of skin, eyes, muscles, GIT…
- HBV associated.
Diagnosis:
- Anemia, high ESR
- Sural nerve biopsy
Treatment: steroid and cyclophosphamide.

205
5) Henoch – Schonlein purura.
- Systemic deposition of IgA in multiple tissues
- Most accurate test: biopsy
-treatment: supportive as resolves spontaneously.
6) IgA – nephropathy (Berger disease)
- After viral illness develops hematuria 1-2 days
- like HSP IgA deposition however symptoms only from kidney.
Diagnosis:
- IgA high:
- Complement levels normal

- Biopsy >> IgA in kidney.
Treatment:
- Proteinuria: ACE inhibitors, ARB

- Massive proteinuria: Steroids.
7) Post infectious glomerulonephritis
etiology: group A B-hemolytic streptococci(strept pyogens)
clinical pictures:
- smoky, cola, tea- colored Urine
- Hematuria, red cell cast, proteinuria.
- Periorbitial edema, HTN.
Diagnosis:
- Antistreptolysin test and antihyaluronic acid test.

- Complement level C3 low.
- Renal biopsy >> IgG+C3 deposited in the mesangium.
Treatment:
- Diuretics for HTN

- Antibiotics for organism.
206
8) Thrombotic thrombocytopenic purpura AND Hemolytic uremic

syndrome
HUS: E. coli 0157: H7 food poisoning.
- Hemolytic anemia, Uremia, thrombocytopenia

- Treated by plasmapheresis don’t give antibiotic or transfuse platelets.
TTP: Idiopathic disease associated with HIV

- Hemolytic anemia, uremia, thrombocytopenia
- Treated by plasmapheresis, dipyridamole preventing platelet aggregation.
9) Cryoglobulinemia
- Type of vasculitis
-associated HCV
- renal disease, joint pain, neuropathy, skin lesions
- no GIT involvement.
High ESR, low complement, test for cryoglobalins
treat with interferon + ribavirin >>HBV
plus doses steroids +plasmapheresis.
10) Diabetes:
- Microalbuminurina < 300 mg.
Treatment: by ACE inhibitor or ARB.
11) SLE
12) Alport syndrome.
- Glomerular disease + congenital eye + ear abnormality

207
13) Idiopathic rapidly progressive glomerulonephritis
- Associated with crescent formation
- ANCA negative
- Diagnosis: biopsy
- Treatment: steroids and cyclophosphamide
14) Amyloidosis:
2 Type:
1) AL: plasma cell dyscrasia >> associated with multiple myeloma.

2) AA: proteinaceaus material associated with RA, IBS, MM.
Clinical pictures:
- Glomerulonephritis, restrictive cardiomyopathy large tongue, carpal tunnel
syndrome, Malabsorption.
- Amyloid protein build up in kidney, GIT, nerves, muscle, heart,
Diagnosis:
- biopsy of organ With congo red >>green birefringence.
Treatment:
Melphalan + prednisone:
Nephrotic syndrome:
- Renal disease sufficient to produce level of proteinuria > 3.5 g /24 hour,
Hyperlipidemia, edema, low serum albumin.
Clinical picture:
1) Edema: because 1) increase salt and water retention

2) low oncotic pressure in serum.
2) Hyperlipidemia: because loss of lipoproteins or signals on surface of chylomicrons

and LDL
3) hyperlipiduria

208
4) Hypercoagulable states: because loss of anticoagulant proteins such as

antithrombin, protein C, protein S >> arterial and venous thrombosis.
5) Mineral deficiency (iron, zinc, copper) because loss of their transport protein
(transferrin and ceruloplasmin)
Diagnosis:
1) 24hour urine > 3.5 g protein (difficult)

2) Single spot urine for albumin and Creatinine (easy)
3) Immune electrophoresis to detect Bence – Jonse protein.
4) Renal biopsy: most accurate.
Treatment:
1) Steroids.
2) Cyclophosphamide or mycophenolate.
3) ACE inhibitors or ARAB for proteinuria.
Classifications:
1) Membranes:
- Associated with lymphoma, breast CA, endocarditis.HBV, HCV, SLE,
penicillamin, NSAIDS>
2) NIL lesions (Minimal change disease)

- Most common in children
- Light microscopy normal but election microscopy sees fusion of foot processes.
3) Mesangial:
- idiopathic, steroid resistant
- immunofluorescent staining show IgM deposits in expanded mesangium.
4) Membrainoprolifrative:
- Associated with chronic hepatitis and low complement
5) Focal – segmental:
- most common in adult
- Associated with heroin and HIV
- Limited response to steroids.

209
DIAGNOSTIC TESTING IN RENAL DISEASE:

1) Urinalysis
2) Proteinuria
- Microalbuminuria: 30- 300 mg/24 hour.
- Mild proteinuria < 1 gram / 24 hour
- Orthostatic proteinuria. No protein in first 8 hour. then find it >>benign
condition.
3) Hematuria: (red cell in urine)
- Stones, cancer, bleeding, disorder, trauma, cyclophosphamide, infection.
4) Nitrites: marker of infection of gram negative bacteria.
5) Bacteriuria: bacteria in Urine.
- Limited significance except pregnant women
END – STAGE RENAL DISEASE / DIALYSIS ( CHRONIC

RENAL FAILURE )
- Most common cause of ESRD = DM and HTN
- Most common used dialysis = hemodialysis
- Most common complication of peritoneal dialysis is peritonitis.
Complication of ESRD
1) Anemia: because loss of erythropoietin
Treated by replacement of erythropoietin.
2) Hypo Ca/ Hyper PO4:
Causes :
1) a loss of 1.25 dihydroxyvitamin D:

210
2) Inabilities of the kidney to excrete phosphate.
Treatment:
1) Vit D replacement.
2) Phosphate binders: calcium carbonats, calcium acetate
- Sevelamer, lanthanum phosphate binder doesn't contain ca used in abnormally
high Ca.
3) Cinacalcet shut off parathyroid to decrease PO4.
3) Osteodystrophy: (osteitis fibrosa cystica)

- Low 1.25 vit D >>low Ca >>high parathyroid >> removing Ca from bone
- Acidosis removing Ca from bone.
4) HyperMg:
- Because decrease renal excretion treated by magnesium intake restriction.
5) HTN and accelerated atherosclerosis:

- most common cause of death.
6) infection:
- uremia inhibits neutrophils.
- most common organism is staph because constant penetration of skin by dialysis.
7) Bleeding:
Causes:
1) Urinary loss of protein C, S and antithrombin.
2) Uremia induced platelet dysfunction >> treated by desmopressin
8) Dietary treatment:
- Restrict potassium, sodium, protein, Mg, Po4
9) Others: pruritus, hyperuricemia, decrease libido from low testosterone,

weakness, fatigue, glucose intolerance.
Indication of Dialysis:
1) Hyperkalemia > 7.0 mmol/L
2) Acidosis ph <7.2
3) Fluid over load
4) encephalopathy
5) Pericarditis.
6) BUN > 70 mg/dl
7) refractory HTN / pulmonary edema
211
Stage of CKD
>= 90
Stage 1
60-90
Stage 2
30-60
Stage 3
15-30
Stage 4
<15 need dialysis or renal transplant
Stage 5 (ESDR)
FLUID AND ELECTROLYTE

Hyponatremia
- Na<135 mEq
- Na is the main Extracellular cation
Etiology:
I- pseudoHyponatremia (normal total Na body level but blood level is low):

1- Hyperglycemia: increase 100 mg /dl >>> decrease 1.6 Na mEq/L.
2- Hyperlipidemia lab artifact.
II- Hypervolemic states (increase EFC):

1- CHF.
2- Nephrotic syndrome and low albumin level.
3- Cirrhosis.
4- Renal insufficiency.
III- Hypovolemic states.(Decrease EFC)

1- GIT: vomiting, diarrhea.,gastric suction
2- Skin loss: burn, sweating, cystic fibrosis.
3- Diuretics.
4- Renal Na loss.
5- Adrenal inhibitors (Addison disease).
6- ACE inhibitors.
Euvolemic states:
1- psychogenic polydipsia:
2- Hypothyroidism.
3- Diuretics.
4- ACE inhibitor.
5- Endurance Exercise.
6- SIADH.

212
Clinical picture:
-confusion, Forgetfulness, disorientation, seizure, coma symptoms depend on how
Fast Na drops.
Treatment:
- Mild hypoNa: fluid restriction.
- Moderate hypoNa:N/S +diuretics(Furosemide)
- Sever. HypoNa: IV 3% hypertonic saline or V2 receptor antagonists
conivaptan,tolvaptan
Note: rate of correction for Na is 0.5-1 mEq / hour if faster than that >>central
pontine Myelinolysis.
Hypernatremia
-Na>145 mEq l
Etiology:
1- Insensible losses, without intake hypotonic fluids:(burns,sweating, fever,
exercise)
2- GIT: diarrhea
3- Transcellular shift: Rabdomyolysis,seizures
4- Renal: Diabetes insipidus, idiopathic, Trauma, infection,hypoxic brain damage,
Osmotic, dieresis
Clinical pictures: lethargy,weakness irritability, seizure, coma.
Diagnosis: to distinguish between Nephrogenic and central Diabetes insipidus give

ADH.
Treatment: isotonic IV fluids
Note: correction of Na should 1 mEq /L every 2Hr if faster than that >>cerebral
edema.

213
Hypokalemia:
- K < 3.5 mEq/L
- K is the main intracellular cation
Etiology:
1- GIT: vomiting,diarrhea, tube drainage.
2- Transcellular shift: alkalosis, insulin,beta agonist vit B12 replacement
3- Urinary losses, Diuretics, increase aldosterone, low magnesium levels.
Clinical Picture:
Muscle: weakness,paralysis
Heart: arrhythmias >>fatal
Diagnosis: EGG >> flat T wave,U wave
Treatment:
- IV maximum (10-20 mEq / h) don't use dextrose

- Oral
Hyperkalemia:
Etiology:
1- increase intake
2- Extracellular shift
- Pseudohyperkalemia: hemolysis, trauma
- Acidosis.
- Insulin deficiency.
- Tissue breakdown: Rabdomyolysis,seizure.
-periodic paralysis
3- Decrease Urinary excretion

-renal failure
-Hypoaldosteronism:
-primary adrenal insufficiency.(Addison)
-k-sparing diuretics amiloride, spironolactone.
-NSAIDS
Clinical picture,
Muscle: weakness
214
Heart: arrhythmia >>fatal
Diagnosis: ECG: peaked T waves, widened QRS, Short QT, prolonged PR.
Treatment:
1-calcium chloride: to protect heart.
2-Na Hco3: Don’t give in same IV with calcium.
3-insulin + Glucose: 30-60 min to work.
4-Diuretics,beta agonists.
5-cation exchange resin (kayexalate): only treatment remove K from body by GIT.
6- Dialysis

215
ACID / BASE DISTURBANCE
Alkalosis (high PH)
Metabolic
Etiology:
1- H Ion loss:
-Exogenous steroids
-GI loss (vomiting, NG Tube)
-Renal loss (Conn syndrome,
Cushing,ACTH, licorice)
-Decreased chloride intake
-Diuretics
2-HCO3 retention:
-Hco2 administration
-contraction alkalosis
-Milk alkali syndrome
3-H+ movement into cell:

Hypokalemia.

216
Respiratory:
(Hyperventilation)
-anemia, pulmonary embolus, sarcoid, anxiety,pain.
-Progesterone, catecholamines, hypoxia, cirrhosis,pregnancy, salicylates
Acidosis (low PH)
Metabolic:
According to anion Gap = (Na+)-(HCO3-+CL-)= 8-12
I- Low Anion gap

1- myeloma
2- low albumin level
3- lithium
II- Normal Anion gap:

1-Diarrhea
2-Renal tubular acidosis
3-Ureterosigmoidostomy
II- increased anion gap: LA MUD PIE

L: Lactate(sepsis, Ischemia)
A:Aspirin
M: Methanol
U:Uremia
D:DKA
P:Paraldehyde, propylene glycol
I:Isopropyl alcohol, INH
E:Ethylene glycol
Respiratory (Hypoventilation)
-COPD
-Pickwickian
-obesity
-suffocation
-opiates
-sleep Apnea
-kyphoscoliosis
-myopathies
-Neuropathy
-Effusion
-Aspiration

217
‫‪Chapter 7 : Nephrology‬‬

‫‪218‬‬
RENAL TUBULAR ACIDOSIS

Distal (type 1)
Etiology:
1- Sporadic
2- Autoimmune disease (SLE, S jogrense syndrome)
3- Drugs: amphotericin, lithium, analgesics,
4- Nephrocalcinosis, sickle cell, chronic infect
5- Familial
6- Chronic hepatitis.
Clinical picture:
- Urine PH > 5.3
- Hypoaldosteronism + hypok
- Nephrocalcinosis, nephrolithiasis
Diagnosis: (Acid load test) >> give ammonium chloride)
- RTA >> NH4Cl in urine will be low + urinary anion gap will be positive.
- Diarrhea >> NH4Cl in urine will be high + urinary anion gap will be negative.
Treatment
- Oral HCO3 - Potassium citrate.
Proximal (Type II)
Etiology:
- fanconi syndrome, Wilson disease, Amyloidosis, myeloma, acetazolamide, vit D
deficiency, hyperparathyroidism,chronic hypoca, heavy metals, chronic hepatitis,
autoimmune (SLE, sjogren syndrome)
Clinical pictures:
- Basic urine (body loses HCO3-)>> urine acidic
- Hypok + HCO3- (18-20) + leak of glucose, amino acid phosphate.
- Bone disease: osteomalacia + rickets
Diagnosis:
- Basic urine + acidemia
Treatment:
- Potassium
- Thiazides + HCO3-

219
Hyporeninemic / Hypoaldosteronism (type IV)
Etiology:
- Aldosterone deficiency
- DM
- Addison disease
- Sick cell disease.
- Renal insufficiency
Clinical picture:
- Hyperk
- Mild- mode renal insufficiency
- Hyperchloremic metabolic acidosis (non-anion gap)
Diagnosis: high urine Na with salt restriction
Treatment: fludrocortisones
NEPHROLIIHIASIS
Etiology:
1- Calcium oxalate (most common)
2- Calcium phosphate
3- Mg/ aluminum / phosphate (struvite)
4- Urine acid
5- Cysteine
6- Indinavir
Hypercalciuria:
1. Increased absorption
- Vit D intoxication
- Familial
- Increased vit D with sarcoid and other granulomatous disease
2. Idiopathic renal Hypercalciuria
3. Resorptive
- Hyperparathyroidism
- Multiple myeloma
Hyperoxaluria:
- Familial
- Enteric (IBD)

220
Hypocitraturia:
Uric acid stones:
- Gout, hematologic,malignancies, crohn's disease

- Cystinuria, genetic disease
- Infection, urease – producing organisms (proteus)
Clinical pictures:
Constant flank pain, hematuria, pain radiating to groin.
Diagnosis:
- X- ray, U/S
- Serum and Urine Ca
- Spiral CT scan
Treatment:
1- Analgesia, hydration, bed rest.

2- Shock wave < 2 cm
3- Ureteroscopy.
4- Percutaneous, removal
5- Borderline. Sized stone 5-7 mm >> nifedipine + tamsulosin.
HYPERTENSION
Essential Hypertension:
- Systolic blood pressure > 140 mm Hg

- Diastolic > 90 mm Hg

221
Risk Factor:
-Age - men - Black
Clinical pictures:
- Asymptomatic found on routine examination

- Symptoms:
1) Acute symptoms with hypertension emergency
2) complications from end - organ damage.
Hypertensive emergency: Hypertensive urgency :

SBP >= 180 or DBP >=110
- Signs and symptoms of plus
No target organ damage
- (cardiac, neurologic, renal, retinal).
Long – term (complication)
1) Cardiac: myocardial ischemia, CHF, aortic aneurysm

2) Cerebovascular: TIA,stoke
3) Renal : proteinuria, Hematuria, high BUN, Cr.
4) Retinopathy: Hemorrhages, exudates, narrowing papilledema.
Secondary Hypertension: (from other disease)
Diagnosis:
Prior labeling patient the following steps are
necessary:
1- Allow the pt to sit quietly for 5 min

2- Never label patient as hypertension after
only single reading.
3- Repeat the reading 3-6 times over several
months.
Laboratory investigation:
1- Urinalysis, protein, glucose, red blood cell

2- HematoCrit
3- Serum potassium
4- Bun/ Cr
5- ECG
6- Glucose, lipid

222
Treatment:
1) Non -pharmacologic modifications

- Weight reduction
- Dietary Na restriction
- aerobic exercise
- Avoid alcohol intake
- Dietary modification: low fat diet, increase dietary fiber, DASH plan.
2) Pharmacologic:
Start medication after 3-6 month of non pharmacologic therapy and still > 90 mmHg
General principles:
- In absence of indication or contraindication use

i. A: ACE, ARBs
ii. B: B B
iii. CC: calcium chamnles block
iv. D: diuretics
- HTN > 160/100 use 2 drug initially
Specific hypertensive therapy:

1. DM >>ACE, ARBs
2. Post MI >>BB
3. Left ventricular failure >>ACE inhibitor, BB
4. African – American pt. are least effectively with ACE
5. Pregnant pt >> alphamethyldopa, labetalolo, Hydralazine, CCB
6. Bengin prostatic hyperplasia >> tamsulosin
7. Proteinuria >> ACE inhibitor
8. Emergency HTN >> vasodilator
9. Pheochromocytoma >> phentolamine, phenoxybenzamine
10. Kidney stone >> thiazides
Hypertensive emergencies (malignant / accelerated HTN ) :
- Acute onset of serve HTN and rapidly worsening symptoms of end –organ
damage > 120-130 mm Hg
(Note: malignant HTN: Encephalopathy or nephropathy with papilledema)
etiology: unknown
Clinical picture:

223
1) Neurologic: encephalopathy, headache, confusion, seizures.

2) Cardiac: chest pain, MI, palpitations, Dyspnea.
3) nephropathy Hematuria, proteinuria, renal failure
4) retinopathy: papilledema, hemorrhages, blurred vision.
Diagnosis: CT, ECG, Lab.
Treatment:
- IV therapy:Nitroprusside and labetalolo

- IV ACE inhibitor: Enalaprilat
- The most important point not lowers pressure more than 25% within 1-2 hour.
Secondary Hypertension:
- HTN in the presence of underlying cause
- The following should be screened for 2nd HTN

1) Very old or very young (<25/>55)
2) Feature of history, physical Ex, lab With particular form
3) Pt who remain HTN despite increasing dosages and number of antihypertensive.
1) Renal artery stenosis:
Etiology :
1- Atherosclerotic disease in elderly.
2- Fibromuscular dysplasia in women
Presentation: upper abdominal bruit
Diagnosis:
1) U/S initial test
2) captopril renogram: decrease GFR after captopril.
3)Arteriogram: confirmation:
4) Duplex and MRA
Treatment:
- Initial treatment ; Percutaneous transluminal angioplasty

- If fail surgical resection
- ACE inhibitor last resort

224
2) Primary hyperaldosteronism (conn syndrome)
Etiology: - most common cause adenoma
- Presentation
1. HTN + Hypok
2. symptoms of Hypok: muscular weakness, polyuria,polydipsia.
Diagnosis: high aldosterone
Treatment:
- surgical>> adenoma - K- sparing diuretics: spironolactone.
3) Pheochromocytoma:
- episodic HTN, headaches, sweating, palpitation, tachycardia.

Diagnosis,
1) Initially VMA, metanephines, catecholamines in urine.

2) CT MRI to localize the tumor
Treatment : alpha + B blocker + surgical removal
4) cushing disease:
- hypertension + cushingoid manifestation
Diagnois : Dexamethasone suppression test + 24 hour urine cortisol
Treatment: surgical resection.
5) Coarctation of aorta
- HTN upper extremities
6) Miscellaneous:
OCP, acromegaly, congenital adrenal enzyme deficiencies, causes of chronic renal

disease.

225
ANTIHYPERTENSIVE MEDICATIONS
1) Diuretics.
Thiazides Loop k-sparing
Hydrochlorothiazide Spironolactone,
Furosemide (lasix)
chlorothiazide, Eplerenone,
Examples Ethacrynic acid,
Metolazone, Amiloride,
bumetanide, torsemide
indapamide Triamterene
Distal tubule
Site of
Distal tubule Loop of henle (Aldosterone
action
antagonist)
4 hyper glucose 4 hypo
1-hyperglycemia 1-hypoNa
2-hyperlipidemia 2-hypoK 1-hyperK
Side effect 3-hyperuricemia 3- hypovolemia 2-gynecomastia for
4-hypercalcemia 4-hypoH+>>alkalosis spironolactone
5-hypoCa for loop
Relative Contraindications. Diabetes, gout, Hyperlipidemia.
2) Beta blockers.
Selective B1 blocker Non-Selective(B1+B2) blocker
-Atenolol -Propranolol
Drugs -metoprolol -Labetalol, carvedilol(alpha 1
-bisoprolol blocker
-acebutalol
Block B1>> Block B1 >> same
Mechanism 1- decrease HR Block B2>>
2- decrease 1- vasoconstriction
contractility 2- bronchoconstriction
3- slow conduction of
AV node
Bradycardia,bronchospasm,vasospasm,hyperglycemia,
Side effect masking hypoglycemia, hyperkalemia, impotence,
hypotension, depression
Sinus bradycardia, heart block, WPW syndrome, hypotension,
Contraindication bronchial asthma, CHF, DM, chronic ischemia

226
3) ACE inhibitor
Side effect cough, angioneurotic edema, neutropenia, taste disturbances, anaphylactic

reactions.
Relative Contraindications: Less effective in African-American patients.
Absolute Contraindications: Bilateral renal artery stenosis, pregnancy.
4) Calcium channel blocker
Non-dihydropyridines Dihydropyridines
Drug 1-Diltiazem 1-Amlodipine
2-Verapamil 2-Nifedipine
3-Felodipine
Mechanism Block smooth muscle + Block smooth muscle Ca
myocardial Ca channel channels
>> slow AV conduction >> vasodilation of coronary
>> decrease HR and peripheral vessls
>> vasodilation of coronary and
peripheral vessls
Side effect 1-Hypotension 1-hypotension
2-bradycardia 2-reflex tachycardia
3-ankle edema( most common) 3-ankle edema( most common
4-flushing
5-gingival hypertrophy
Contraindication Bradycardia, heart block, Hypotension, CHF, sever AS,
hypotension, WPW syndrome , liver failure
CHF
5) ARB
Major Side Effects: Few. This is the newest class of antihypertensives.

Absolute Contraindications: Pregnancy.

227
6) Central – acting sympatholytics
Major Side Effects: Depression, fatigue, dry mouth, impotence, Bradycardia, heart
block, memory loss. Methyldopa gives hepatitis and Coombs-positive hemolytic
anemia.
Relative Contraindications: Elderly or depressed patients.
7) Direct vasodilators
Major Side Effects:
• Minoxidil gives marked fluid retention, pericardial effusion, and hirsutism
• Hydralazine gives a lupus-like syndrome
Relative Contraindications: Angina pectoris.
8) Alpha – Blocker
Side effect: syncope first dose, dizziness, headache.

228
Chapter 8
Pulmonology

229

230
DIAGNOSTIC TESTS
Pulmonary Function Tests
PFT :
Restrictive diseases :
Low TLC, low RV low VC
Obstructive disease :
Low FEV 1 /FVC low FEF25 -75
high RV high TCL
Lung volumes
Forced Expiratory Volume (FEVs)
- FVC: total amount of air expired during forced expiration

- FEV1: amount of air expired during forced expiration in the first second
- FEF 25-75 = FEV1/ FVC
Carbon monoxide diffusing capacity (DLco):
- Measures the ability of the lungs to perform gas exchange.

- Decrease in: - emphysema - interstitial lung disease -mild HF
- Normal: -chronic bronchitis - Extra pulmonary restrictive disease
- Increase: good pasture syndrome
Methacholine challenge disease:
- Bronchoprovocation with Methacholine to asses cough or wheezing

- PFT after and before Methacholine
- Positive If FEV < 20 %

231
Bronchodilator reversibility:
- PFT after bronchodilator

- If PFT improved > 12% >>
obstructive lung disease
Flow volume Loops:
- Restrictive lung disease: shift to the right)

- obstructive lung disease: alteration on the y-axis)
- Tracheal stenosis after prolong intubation volume loop: flattened on the top and
bottom.
- Vocal cord paralysis: loop flattened in bottom
Disturbances in Gas Exchange

- Alveolar – arterial gradient (PAO2-Pao2gradient) is useful in the assessment of
oxygenation.
- increase in all causes of hypoxemia expect hypoventilation and high altitude
Oxygen –hemoglobin dissociation curve

- it is S shaped curve at PO2 60 mmHg
the O2 sat is 92%
- when PO2> 60 mmHg there is small
increase in O2 sat
- when PO2 < 60mmHg there is rapid
decrease in O2 sat
- increase CADET shift curve to the
right
- decrease CADET shift curve to the
left
- CADET: CO2, Acid, 2.3-
DPG,Exercise,Temperature
- curve shift to the right means less Hb binding to O2 and more O2 delivered to
tissue
- curve shift to the left means more Hb binding to O2 and less O2 delivered to tissue

232
Pulmonary Nodule
Prior x ray
No prior x ray
High risk pt low risk pt
Open - lung biopsy and Chest x -rays or chest CT

every 3 months for 2 years
removed of the nodule
stop the follow up if after 2
at the same time. years there is no growth .
- low-risk patients < 35 years of age and nonsmokers with calcified nodules,
- High - risk patients > 50 years of age with a smoking history and nodule are
likely to have born-congenic cancer
Pleural Effusion
- The accumulation of fluid in the pleural cavity. It is either transudative or exudative.

233
Etiology:
Diagnosis:
- How do we make the distinction between these two?

1- Thoracocentesis get 2 tests from the thoracentesis fluid – lactate dehydrogenase
and protein-
2- Get 2 tests from the serum – LDH and protein.
- If the least one criterion is not met, then this is an exudative effusion.
Parapneumonic effusion:
Etiology: bacterial pneumonia
Diagnosis: a Thoracocentesis is mandatory also in this setting to rule out a

complicated parapneumonic effusion (because of the possibility of progression to an
empyema)
Treatment: An empyema (or complicated effusion) needs chest-tube draining to

resolve, while an uncomplicated parapneumonic effusion responds to antibiotics
alone.

234
Malignant pleural effusion:
Etiology: most common causes >> lung cancer, breast cancer, and lymphoma.
Diagnosis: Thoracocentesis with cytological Ex
Note: B-type natriuretic Peptide: BNP is a very sensitive test for heart failure, it is not
specific.
VENTILATION
1- Noninvasive ventilation (no intubation)
Bi –level positive airway Continuous positive airway

pressure pressure
Mechanism Delivers pressure at Supply air pressure on continuous

alternating level: basis:
Higher for inspiration and Allowing airway continuously be

lower for expiration opened
1- Obstructive sleep apnea
Uses 1- COPD 2- Preterm infants with
2- Acute respiratory failure underdeveloped lung
(pneumonia asthma …) 3- CHF with pulmonary edema
3- Chronic respiratory 4- Near drowning
failure 5- Home O2 deliver (portable
CPAP)
2- Invasive ventilation (intubation)

- Used for hypoxemia and respiratory failure
- Positive end – expiratory pressure (PEEP): is the alveolar pressure above
atmospheric pressure
- PEEP (4-5 cm H2O) is used at beginning of ventilation
- Complication of PEEP: decrease venous return, pulmonary barotrauma, renal
dysfunction, electrolyte imbalance

235
OBSTRUCTIVE DISEASES:
Asthma:
Definition: inflammatory hyper reactivity of the respiratory tree to various stimuli,

resulting in reversible airway obstruction.
Etiology:
2- Extrinsic
1- Intrinsic or Idiosyncratic (allergic, atopic)
(non atopic)
-secondary to non-immunologic stimuli, -specific immunologic (IgE) class

such as infections irritating inhalation, type1 are produced.
cold air, exercise, and emotional upset
-is precipitated by allergens
-attacks are severe.
-other symptoms include allergic
rhinitis and eczema
Note:
- Respiratory infections are the most common stimuli to cause asthma exacerbations
(respiratory syncytial virus in young children, rhinoviruses in adults)
- Pharmacologic stimuli: most common are aspirin, coloring agents such as
tartrazine and B-adrenergic antagonists.
- Aspirin sensitivity – nasal polyposis syndrome affects adults. Starts usually with
perennial vasomotor rhinitis later, Asthma occurs with minimal ingestion of aspirin
and similar>> cause chronic overexcretion of Leukotrienes, which activate the
mast cells.

236
Pathophysiology:
- Mediators released histamine, bradykinin Leukotrienes (LTs) C, D, and E and
prostaglandins (PGs) E2 F2 andD2 >>bronchoconstriction and vascular
congestion.
- Cells play role in the inflammatory response: mast cells, lymphocytes, eosinophils.
Clinical pictures:
- Mild attack: slight tachypnea, tachycardia, prolonged expirations, mild diffuse
wheezing is seen.
- Severe attack: accessory muscles of respirations, diminished breath sounds, loud
wheezing, hyper resonance, and intercostals retraction are noted.
- Poor prognostic factors: fatigue, diaphoresis, pulsus paradoxus (>20mmhg)
inaudible breath sounds, decrease wheezing cyanosis and bradycardia.
- Variants of asthma: nocturnal cough, exercise induced asthma.
Diagnoses:
1- ABG ;
- Acute phase: low paco2, high pH, low pao2.
- severe asthma or status asthmaticus: high paco2, low PH, low pao2
2- Chest x- ray: nonspecific to ruling out acute infection
3- PFTs:
- Bronchodilator reversibility: improve (FEV1) 12% and 200ml with b2-
adrenergicagonist)
- Provocative challenge (Methacholine /cold air challenge test): decrease In
FEV/FVC or FEF25-75 of 20% .
Treatment: ‫سنقو بذكر كل انواع االدويه المستخدمه في عالج الربو لكن بضعها ال يستخد دائما‬
1- B-adrenergic agonist (albuterol,terbutaline)
- Mainstay of treatment in acute and chronic asthma.
- Salmetrol is a long lasting (12h) type of albuterol that is effective in nocturnal
cough variant and exercise – induced asthma.
- side effect:
a- tremor (most common)
b- Tachycardia
c- excessive sweating
d- anxiety
e- insomnia
f- agitation
- used with caution in patients with cardiovascular disorders, hypothyroidism,
diabetes mellitus, hypertension and coronary insufficiency
2- Aminophylline (ethylenediamine salt of theophylline)
- improve contractility of the diaphragm as well as other respiratory muscles

237
- They are not routinely used in asthma.

3- Anticholinergic drug (ipratropium bromide and tiotropium):
- Disadvantages: take significant time to achieve maximal bronchodilation -90 min.
4- O 2: Supplemental oxygen by nasal cannula or mask given immediately.
5- Antibiotic: in patients with symptoms (purulent sputum) and chest x-ray finding
(infiltrates)
6- Inhaled corticosteroids:
- Is the cornerstone of chronic asthma therapy in adults?
- Side effects of inhaled corticosteroids:
a- oral candidiasis
b- glaucoma
c- cataracts
d- diabetes
e- muscle weakness
f- Osteoporosis.
7- Systemic steroids: are used only in acute exacerbation (for 10-14 days) and chronic
severe asthma
8- Leukotrienes modifiers: inhibit 5- lipoxygenase (the enzyme involved in
leukotrienes production) 2 type:
a- Leukotrienes inhibitor: zileuton
b- Receptor antagonists: zafirlukast, montelukast
9- Mast cell stabilizers (Cromolyn and Nedocrmil)
- are used extensively in the chronic treatment of pediatric asthma.
ACUTE treatment:
1- O2
2- B agonist
3- Anticholinergic
4- Steroid IV then oral

238
Chronic treatment:
Type Symptoms Treatment
-symptoms 2 times/week
- night symptoms rare (1-
Mild short acting B- agonist PRN
2nights month)
- FEV: normal > 80%
-Symptoms most of the
-short acting B- agonist PRN
week or daily
-inhaled steroid
Moderate -night symptoms least 5
-long B agonist for nocturnal
nights
symptoms
-FEV1 60-80%
-Short acting B- agonists PRN

-Symptoms daily -inhaled steroids,
Severe -Night symptoms frequent - long beta agonists
-FEV < 60 % -antileukotriene
-oral steroid (lowest dose possible).
Allergic Bronchopulmonary Aspergillosis
Etiology: allergic lung reaction to fungus (Aspergillus fumigates)in asthma or cystic

fibrosis patients
Clinical pictures:
1- Progressive symptoms of asthma: wheezing, SOB, fever
2- Decrease appetite
3- Brownish flecks or plugs in sputum
Diagnosis:
1- X ray: new or migrating pneumonia
2- High Eosinophils
3- High antibodies to Aspergillus
4- High IgE
5- Skin test: shows if pt allergic to Aspergillus
Treatment: corticosteroids

239
Chronic Obstructive Pulmonary Disease (COPD)
Definition: includes patients with emphysema and chronic bronchitis.
- Chronic bronchitis have productive

cough for most days of a 3 month
period for at least 2 consecutive years.
- Emphysema patients have abnormal
permanent dilation of air spaces distal
to the terminal bronchioles with
destruction of air space walls.
- Nonreversible obstruction of the
airways.
Etiology:
1- Cigarette smoking: 20 pack years of tobacco exposure.

2- Alpha -1- antitrypsin deficiency: autosomal recessive disease >> emphysema and
liver abnormalities.
Pathogenesis: long term exposure to cigarette smoke >> inflammatory cells are
recruited in the lungs. >> secrete proteinases >>air space destruction + permanent
enlargement + decrease elastic recoil (mainly in emphysema) and increased airway
resistance (chronic bronchitis) occur.
Physical Examination:
- emphysema: distant breath sounds will be heard on
auscultation
- Chronic bronchitis: rhonchi and wheezes to
auscultation.
- right heart failure (cor pulmonale)
- clubbing
Diagnosis:
1- Chest x-ray:
-chronic bronchitis =increased pulmonary marking
- Emphysemas = hyperinflation of bilateral lung fields
with diaphragm flattening small heart size.
2- PFT: are the diagnostic test of choice
- low FEV 1/FVC ratio and FEF25-75
- High RV and TLC.
- Low DLco: Emphysema
- normal DLco: chronic bronchitis
- After bronchodilator FEV / FVC to remain the same.
240
Complications:
- hypoxemia with nocturnal desaturation

- erythrocytosis
- pulmonary hypertension
- cor pulmonale, right heart failure.
Management of stable phase COPDs:
1- Anticholinergics (ipratropium bromide, tiotropium): first line drugs

2- B-adrenergic agonists (albuterol) are not first line agents because many of the
patients have underlying heart disease.
3- Theophylline: a xanthine derivative has significant toxicity
- Symptoms: nausea and vomiting, palpations, tremulousness, death from cardiac
arrhythmias.
- Drug interactions with theophylline level: increase with fluoroquinolones,
clarithromycin, H2-blockers, certain beta blockers and calcium channel blockers
- Decrease with rifampin, Dilantin, phenobarbital and smoking.
4- Home Oxygen therapy with hypoxemia: keep the O2 saturation > 90%.
5- Smoking cessation
6- Vaccine: pneumococcus (pneumovax), H. influenza.
Acute Setting Treatment (Exacerbation)
- precipitating factor for COPD exacerbation:

A. viral lung infections (most common)
B. bacterial infections
C. heart failure
D. myocardial ischemia
E. pulmonary embolism,
F. lung cancer
G. esophageal reflux disease
H. Medications: BB
- Initial management:
1- O2 saturation: pulse oximetry.
2-Arterial blood gas (ABG): hypercapnia
3- Chest x-ray: pneumonia.
4- Spirometry: NOT helpful in COPD exacerbation
5- Theophylline level
6- CBC, ECG.
241
7- Admission to the hospital.
8- Intubation and mechanical ventilation: decreased levels of consciousness, cyanosis

or hemodynamic instability.
Specific Therapy:
1-Oxygen supplementation.
2-Inhaled bronchodilators: most effective medications to improve airway beta –

agonists + Anticholinergic.
3-Systemic corticosteroid, 60 mg prednisone for 2 weeks, intravenous

methylprednisolone then change to oral prednisone
4-Antibiotics despite normal chest radiograms: Macrolides, fluoroquinolones,

cephalosporin, amoxicillin clavulanate.
5-Chest physiotherapy
6-Smoking cessation
7-Teaching the patient optimal use of MDIs.
Prognosis: FEV1 is the best predictor of survival.tobacco cessation is the only means
of slowing progression.
Bronchiectasis:
Definition: the permanent dilation of small

and medium – sized bronchi that results
from destruction of bronchial elastic and
muscular elements,
Etiology:
1-tuberculosis (TB) 2- fungal

infections 3- lung abscess, pneumonia, 4- cystic fibrosis 5-immotile cilia
syndrome (diffuse Bronchiectasis) 6- Kartagener syndrome
Clinical pictures:
1- cough with purulent copious sputum production

2- wheezes or crackles,
3- recurrent pneumonias that commonly involve gram negative bacteria
4- Hypoxemia secondary polycythemia.

242
Diagnosis:
1- Early chest x-ray: in advanced cases

may show 1- 2 cm cysts and crowding
of the bronchi.
2- high resolution CT: best test
Treatment:
1- Bronchodilators,
2- chest physical therapy
3- postural drainage
4- antibiotics such as trimethorprim sulfamethoxazole, amoxicillin and
amoxicillin/clavulanic acid, significant symptoms with intravenous antibiotics.
5- Surgical therapy: patients with localized bronchiectasis
6- pneumococcal vaccine + influenza vaccine
Complications:
1-hemoptysis 2-amyloidosis 3-cor pulmonale 4- visceral abscesses.
INTERSTITIAL LUNG DISEASE

Clinical pictures:
1- exertional Dyspnea
2- nonproductive cough
3- coarse crackles
‫تذكر مع‬
4- pulmonary hypertension, ‫كل االمراض‬
5- The chest x-ray reticular or reticulonodular pattern.
6- PFTs intrapulmonary restrictive pattern.
Causes include:
1- Idiopathic pulmonary fibrosis : Worst prognosis

2- Sarcoidosis
3- Pneumoconiosis and occupational lung disease.
4- Connective tissue or autoimmune disease – related pulmonary fibrosis.
5- Hypersensitivity pneumonitis
6- Eosinophilic granuloma (a.k.a.Langerhan cell histiocytosis)
7- Chronic Eosinophilic pneumonia
8- Wegener granulomatosis.
9- Idiopathic pulmonary hemosiderosis.

243
10- Lymphangioleiomyomatosis
Idiopathic pulmonary fibrosis(IPF)
Definition: inflammatory lung diseases of unknown origin that causes lung fibrosis,
restrictive lung disease
Clinical pictures : As above
Diagnosis:
1- As above
2- high resolution CT scan: ground – glass appearance
3- Lung biopsy is done to exclude other causes.
Treatment: - pirfenidone (antifibrotic) - lung transplants
Sarcoidosis:
Definition: systemic disease of unknown cause, characterized the presence of
nonspecific noncaseating granulomas.
Prevalence: black and patients 20- 40 years of age.
Clinical pictures:
1- pulmonary involvement is most common
2- Ocular, skin, myocardial, rheumatologic, gastrointestinal and neurologic,
manifestations can also occur.
3- Sarcoid syndrome:
. Lofgren syndrome: erythema nodosum, arthritis, and hilar adenopathy
. Heerfordt- Walden storm: fever, parotid enlargement, uveitis and facial palsy.
4- Hilar and left Para tracheal adenopathy is the most common presentation.
Diagnosis:
1- Chest x-ray shows 4 stages of

disease:
Stage 1: bilateral hilar adenopathy
Stage 2: hilar adenopathy with
reticulonodular parenchyma
Stage 3:reticulonodular parenchyma
Stage 4: honeycombing of bilateral
lung fields with fibrosis.
2- Laboratory Finding:
-hypercalcemia or Hypercalciuria : due
to high vitamin D produced by macrophages.
244
- Angiotensin- converting enzyme (ACE) is nonspecific.

- Liver function tests
- PFTs : normal or restrictive pattern.
3- Biopsy :noncaseating granulomas.
Treatment:
- steroids: a high dose for 2 months

- Steroids are mandatory: uveitis, Sarcoidosis involving the CNS, and heart, and
hypercalcemia.
Pneumoconiosis:
Etiology:
- 20-30 years after constant exposure to offending agents (metal, mining of gold,
silver, lead, copper)
Pathology: Alveolar macrophages engulf offending agents >> inflammation and
fibrosis of the lung parenchyma.
Clinical pictures:
1- Dyspnea 2- shortness of breath 3-cough

4-sputum production, 5-cor pulmonale 6- clubbing
Diagnosis:.
1- PFTs show a restrictive pattern with a decreased DLco.

2- Chest x-ray small irregular opacities, interstitial diseases, ground glass
appearance and honeycombing.
3- Hypoxemia is evident with an increased PAo2-Pao2 gradient.
Cool workers
Asbestosis Silicosis
pneumoconiosis
Lobe Lower Upper Upper
diffuse or local pleural

thickening, pleural
CXR Egg shell plaques,calcifications in Small round densities
clacification lower lobe.
Biopsy: barbell shape
fiber
Increase risk of
High IgG IgA, C3, ANA,
bronchogenic cancer Increase risk of TB >> do
Associations RF
(adenocarcinoma, PPD
Caplan syndrome
SCC

245
PLUMONARY THROMBOEMOLSIM
Etiology:
- Arise from proximal (above knee) deep vein thrombi (DVT) in turn
- Most proximal DVT are a consequence of propagation of distal (below – the knee).
- Infrequently occur with upper extremity, subclavian,and internal jugular vein
thrombosis.
- Pregnant patient thrombosis may occur initially in the pelvic veins.
Natural Course: after a proximal DVT dislodges >>vena cava and >>right side of the
heart.>> pulmonary circulation >>obstructing parts of the pulmonary artery
Risk factor:
1- Recent surgery, especially orthopedic surgery (knee replacement surgery.

2- cancer history (prostate, pelvic, abdominal, and breast)
3- Immobile patients (especially those hospitalized)
4- Acquired thrombophilia: lupus anticoagulant,nephritic syndrome, oral
contraceptives.
5- Inherited thrombophilia: factor V Leiden mutation, protein C and S deficiency
and antithrombin III deficiency.
6- Pregnancy and 2 months after delivery.
Clinical Pictures:
- PE:
1- Sudden onset of Dyspnea (most common ) and tachypnea.
2- . Pleuritic chest pain.
3- . Hemoptysis (occur only with infraction).
4- . On exam, always increased respiratory rate with
tachycardia, increased pulmonic sound (p2)
- DVT: thigh or calf swelling with or without

Dyspnea
Wells Criteria: for DVT probability

246
- Symptoms of DVT (3 points)

- No alternative illness that explains symptoms (3 points)
- Immobilization (≥3 days) or surgery in the previous 4 weeks (1.5 points)
- Prior history of DVT or PE (1.5 points)
- Presence of hemoptysis (1 point)
- Presence of malignancy (1 point)
Scoring is done as follows:
- Score >6 = high probability of PE

- Score ≥2 but <6 = mean moderate probability of PE
- Score <2 = low probability of PE
Diagnosis:
- General tests:
1- Arterial blood gas (ABG), hypoxemia with
an elevated A– gradient,
2- Chest x-ray: normal chest x-ray,other
nonspecific findings
-Westermarck sign
-Hampton hump.
3- ECG: sinus tachycardia (most

common finding) + (S1,Q3,T3)(
specific)
- Specific Tests:
1. Pulmonary embolism:
• CT pulmonary angiogram
: initial test
• Ventilation – perfusion
(V/Q)
• Pulmonary angiogram:
gold standard
2. DVT:
• Compression on duplex ultrasound
• Venogram is rarely done
• MRI
3. Both pulmonary embolism and DVT:
• D- dimer is the most sensitive test for thromboembolic disease

247
Treatment : Give oxygen start heparin immediately before the diagnosis is

confirmed. Once the diagnosis is confirmed:
• Heparin – LMWH or unfractionated for 5-7 days(or until INR is therapeutic)

• Warfarin (Coumadin) – be started with heparin and continued for 6 months

248
1. LMWH or fractionated heparin

- inactivates factor Xa
- LMWH is less likely to cause hemorrhage or heparin – induced thrombocytopenia
(HIT).
- HIT is a common complication of heparin treatment and occurs 5-7 days
- Always stop heparin when platelets decrease by a significant amount.
- HIT is treated with the new anticoagulants (argatroban)
2. Warfarin:
- Inhibits the vitamin K dependent factors (II,VII,IX, X = 1972)
- Warfarin dose should be monitored by INR (2-3 to be effective).
- Warfarin skin necrosis is a rare procoagulant effect that occurs in patients who
have preexisting protein C deficiency.
- Anticoagulation is contraindicated in
patients with recent n
eurosurgery or eye surgery.>> inferior
vena cava.
- Warfarin is contraindicated in pregnant
patients >>LMWH
for 6 months is the best alternative
3. Thrombolytics (Tpa, streptokinase):
- used in hemodynamically unstable + massive DVT
4. new class anticoagulants
- Rivaroxaban: factor Xa inhibitor
- Dabigatran: thrombin inhibitor
Note:
• Postthrombotic syndrome (postphlebitic
syndrome)
- is the most common complication DVT
249
- clinical pictures: pain, edema, hyperpigmentation, and skin ulceration,

- Use of compression stocking has prevent the Postthrombotic syndrome.
• No complicated proximal DVTs are usually treated for a total of 6 months.
• In patients with thrombophilias (Hypercoagulable states), lifelong anticoagulation
is considered with warfarin
• Do not check for protein C or protein S deficiency during acute thrombosis
• In patients that develop recurrent thrombosis while on anticoagulants, consider
HIT or cancer – related thrombosis
• Limited distal DVT you have 2 options:
1- monitor for possible extension to the proximal veins by using serial ultrasound
2- treat with anticoagulation for 3 month
• Fat embolism:
- occurs 3 days after long bone fracture, after CPR
- Dyspnea, petechiae (neck and axilla), confusion
- Treatment is supportive (no anticoagulation).
ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)

Definition: acute lung injury that is characterized by increased permeability of the
alveolar – capillary and pulmonary edema
Etiology:
1- Sepsis 2- trauma 3- DIC 4- toxins 5- good pasture

syndrome 6-SLE 7-drowning 8-CABG
Clinical pictures:
1-Dyspnea 2-tachypnea 3- diffuse rales and rhonchi
Diagnosis:
1- Chest x- ray: diffuse interstitial or alveolar

infiltrates
2- ABG: low PaO2, high PCO2
3- Swan – Ganz cath: high pulmonary artery
pressure
Treatment:
1- Treat underling causes

2- Mechanical support + increase positive end-expiratory pressure

250
SLEEP APNEA
- Cessation of airflow > 10 s more than 10 times in hour
Clinical pictures:
1- Somnolence
2- HTN
3- Plu HTN
4- Cor pulmonale
Diagnosis: clinically +polysomnography
2 types:
1- Obstructive sleep apnea:
- Floppy airway
- Obese patient
- Treatment: weight loss, CPAP
2- Central:
- Inadequate ventilatory drive
- Treatment: acetazolamide, progesterone, O2

251
ATELECTASIS
Definition: collapse part or entire lung
Etiology:
1- Postoperative period
2- Mucous plug
3- FB
4- Tumor
Clinical pictures:
1- Tachycardia 2-dyspnea 3-fever 4-

hypoxemia
Diagnosis:
Chest x ray: tracheal deviation, elevation of diaphragm, mediastinal shift
Treatment:
1- Deep breathing and coughing

2- Incentive spirometry and pulmonary toilet
3- Bronchoscopy

252
Respiratory failure
Type 1 respiratory failure Type 2 respiartory failure
Hyperventilation with relatively patent No washout of CO2 either due to

airway washout of CO2 hypoventilation or sever bronchial
obstruction or chest deformity
Decrease PO2 < 60 mmhg with normal Decrease PO2 with increase CO2
or low CO2
Called hypoxemic RF Called hypercapnic RF
Causes: Causes:
1- Emphysema 1- Chronic bronchitis

2- Pneumonia 2- Narcotics
3- Asthma 3- Hypoventilation
4- PE 4- Chest wall abnormalities
5- Plu HTN
6- Bronchiectasis

253

254
Chapter 9
Emergency Medicine

255

256
BASIC LIFE SUPPORT (CARDIOPULMONARY

RESUSCITATION)
1- Assessment of responsiveness of the patient by calling to or gently shaking the
patient
2- call for help (dial 911)
3- CAB (excluding newborns)
4- position the patient on a firm, flat surface
5- and roll the patient so that he or she is face up
6- Check to see if there is a pulse by feeling for at least 5-10 seconds at the carotid
7- chest compressions : ventilations ratio
Number of rescures Chest compression Ventilation
On rescure 30 2
Adult Two rescures 100/min 8-10/min
One rescure 30 2
Children Two rescure 15 2
8- Depth of chest compression 2 in or 5 cm.
:unresponsive ‫اذا لق يت مري ض ال يستجيب‬
‫بصحي المريض عن طريق المناداه والهز الخفيف‬ -1

AED + ‫بطلب المساعده‬ -2
‫ اضع‬,‫ اضع اذني عند انف المريض لتشيك النفس‬:‫بشيك كل شي معبعض‬ -3
‫ فتح مجرى التنفس‬,‫ايدي على نبض المريض‬
:CAB ‫اذا ما في نبض ال تنفس ابدا‬ -4
C: CPR -
A: open airway -
B: give breathing -

257

258
Advanced Cardiac Life Support Algorithms

259
CARDIAC DYSRHYTHMIAS
Asystole
- The complete absence of electrical activity in

the heart.
Clinical Pictures : Person has no pulse.
Diagnosis : observing the rhythm in more than lead on the EKG.
Treatment: (CPR), obtain IV access and prepare the patient for intubation.
1. Transcutaneous pacing
2. 1 mg epinephrine via IV push every 3-5 minutes
Ventricular fibrillation:
- Electrical activity on EKG

with no sing of an organized
pattern.
Clinical picture: Dead person

with ventricular fibrillation on
EKG.
Treatment: The differences between defibrillation and cardioversion are very

important.
• Defibrillation:
- non synchronized delivery of shock at any phase of cardiac cycle
- used in VF and pulseless VT
- During defibrillation you depolarize all of the myocytes simultaneously, hoping
that the SA node will start up normal sinus rhythm.
• Cardioversion:
- shock synchronized with the QRS complex (will not shock untill the QRS )
- If you shock on the T wave you may induce VF.
Post – Resuscitation Care: Hypothermia protocol reduces the risk of this type of
severe neurologic injury.32 – 34 C° (90 – 93 °F) within 6 hours and maintain for 12-
24 hours.

260
Pulseless electrical activity:
- Hypotension to the point of losing one's pulse
Etiology:
1. hypovolemia
2. cardiac tamponade
3. tension pneumothorax
4. massive pulmonary embolism
5. a massive myocardial infarction
6. hypoxia
7. hypothermia
8. potassium disorders
9. acidosis
10. drug: tricyclics, digoxin, beta – blockers or calcium – channel.
Clinical pictures: dead with no pulse.
Diagnosis: pulseless patient normal, activity on the EKG.
Treatment:
- CPR,IV access intubation, and epinephrine

- Do not shock PEA.

261
TOXICOLOGY
Associated physical findings in specific toxidromes
• Miosis: clonidine, barbiturates, opiates, cholinergics, pontine stroke

• Mydriasis: sympathomimetics, anticholinergics
• Dry skin:anticholinergics
• Wet skin: cholinergics, sympathomimetice
• Blisters: barbiturates, carbon monoxide poisoning.
Management of Toxic Ingestions or Overdose
• Induced vomiting within 1-2 hours after ingestion

• Lavage: only useful within the first hour after
ingestion
- Both ipecac and lavage are contraindicated
with the ingestion of acid or alkalis. Charcoal is not used with
PHAILS:
• Charcoal :
-1-2 hour after the ingestion. - Pesticides
- Repeated doses every 2-4 hours. - Heavy metal
- Safe for all patients. - Acids / alkali / alcohol
• Whole bowel irrigation: - Iron
- Large – volume pill ingestions in which - Lithium
the pills can be seen on an x – - Solvents
ray.
• Dialysis: profoundly serious symptoms
such as coma, Drugs need hemodlialysis:
Hypotension or apnea (I STUMBLE)
• Cathartics: used with charcoal
administration. - I: isopropanol
• Forced dieresis: Alkaline dieresis for - S: salicylates
salicylates and Phenobarbital - T: theophylline
• Naloxone/dextrose /thiamine with altered - U: uremia
mental status or coma. - M: methanol
- B: Barbiturates
- L: lithium
- E: ethylene glycol

262
Toxicology screening (tox screen):

- Initial test: urine immunoassay for : alcohol, cocaine, amphetamines,
cannabinoides
- Confirmatory test: Gas chromatography / mass spectromerty
- the time it takes for drugs to clear:
• Alcohol: 3−10 hrs
• Amphetamines: 24−48 hrs
• Barbiturates: up to 6 wks
• Benzodiazepines: up to 6 wks with heavy use
• Cocaine: 2−4 days; up to 10−22 days with high level use
• Codeine: 1−2 days
• Heroin: 1−2 days
• Hydromorphone: 1−2 days
• Methadone: 2−3 days
• Morphine: 1−2 days
• Phencyclidine (PCP): 1−8 days
• Tetrahydrocannabinol (THC): 6−11 wks with heavy use
ACETAMINOPHEN
- 7-10 grams is enough to produce toxicity
- fatalities can occur >12 – 15 grams
Clinical Pictures:
- Stage I (12-24 hour): nausea vomiting gastritis.

- Stage II (24-72 hour): elevation of the transaminases and bilirubin >> clinically
symptomatic signs of liver damage: nausea, jaundice, abdominal pain, hepatic
encephalopathy, renal failure, death.
Diagnosis:
- Clear history of a large volume of acetaminophen ingestion.

- Drug levels are reliable after 4 hours.
- high AST > ALT
- high bilirubin
- High prothrombin time.
Treatment:
1- Activated charcoal.
2- N acetyl cysteine (NAC): within 8 hours of the ingestion.

263
ALCOHOLS
(METHANOL AND ETHYLENE GLYOL)

Etiology:
1- Methanol (wood alcohol): paint thinner, sterno, photocopier fluid, solvents, and
windshield washer solution.
2- Ethylene: automotive antifreeze.
- of the alcohols are metabolized by alcohol dehydrogenase
Methanol formaldehyde, formic acid
Alcohol
dehydrogena
Ethylene glycol
se oxalic acid, oxalate
Clinical pictures:
1- Methanol: visual disturbances blindness.

2- Ethylene glycol: renal failure, stones.
3- Isopropyl alcohol: acidosis in the absence of an elevated anion gap.
Diagnosis:
1- Specific levels of each alcohol are the most specific test.

2- Ethylene glycol: oxalate crystals in the urine, high BUN/Creatinine, fluorescein
to the urine, hypoCa
3- Methanol and ethylene glycol: high serum osmolar gap, metabolic acidosis with
high anion gap.
4- Isopropyl alcohol: osmolar gap without an increased anion gap.
Treatment.
1- Fomepizole (alcohol dehydrogenase inhibitor) is the drug of choice.

2- Dialysis : for coma, seizures, renal failure.

264
CARBON MONOXIDE (CO)
Source: exposure to various forms of burning materials, CO itself is odorless and

tasteless
Metabolism:
- Co binds to hemoglobin 200 times more avidly than oxygen

- Carboxyhemoglobin decreases release of oxygen to tissues and inhibits
mitochondria.
- This results in tissue hypoxia and anaerobic metabolism similar to what would
occur with anemia
Clinical Pictures:
1- Pulmonary :Dyspnea, tachypnea, and shortness of breath

2- Cardiac: chest pain, arrhythmia, and hypotension.
3- Neurologic: Early>> headache (most common), nausea, blurry vision, and
dizziness, >> late >>>confusion, seizures, impaired judgment, syncope.
Diagnosis:
• Carboxyhemoglobin level:
< 10%: Levels up to 10% may occur in city dwellers who are smokers
20 – 30 % Mild symptoms
30 – 50% Moderate to severe symptoms
>50 – 60% May be fatal
• Arterial blood gases or venous blood gases :Metabolic acidosis + pO2 normal
• High CPK.
• Pulse oximetry is not helpful
Treatment
• Removal from source of exposure
• 100% Oxygen administration
• Hyperbaric oxygen in severe cases
Note: Influenza is the most common misdiagnosis entire family presents with “flu”
symptoms without fever, think CO poisoning.

265
CAUSTICS / CORROSIVES (ACIDS AND ALKLI)

Etiology:
1- Acids: toilet, drain, swimming pool, and metal cleaners.

2- Alkali: crystalline lye, dishwasher, hair relaxers, oven
clean
Clinical Pictures: oral pain, drooling, odynophagia, and

abdominal pain..Gastric perforation,
alkali exposures are more serious than acid exposures
Diagnosis:
1- history of exposure
2- Upper endoscopy
Treatment:
1- Immediately wash out the mouth with large volumes of cold water.
2- Irrigate ocular exposures with large volumes of either saline or water,
3- Do not induce emesis, Do not try to neutralize the acid, do not use Charcoal,
steroids or prophylactic antibiotics
DRUGS OF ABUSE
Opiates
clinical pictures :
1- Respiratory depression
2- papillary constriction
3- constipation
4- bradycardia
5- hypothermia
6- hypotension
Treatment: naloxone
Withdrawal of opiates:
• 3-4 hours : fear, anxiety, and drug craving

• 8-14 hours : insomnia, yawning, rhinorrhea, diaphoresis, mydriasis, anxiety
266
• 1-3 days: tremor, muscle spasms, vomiting,diarrhea, tachycardia, chills,

piloerection
- Treatment:methadone or buprenorphine
Cocaine
Pathophysiology: Cocaine blocks the reuptake of norepinephrine and other

catecholamines the synapse
Clinical Pictures:
1- high blood pressure

2- hemorrhagic stroke
3- subarachnoid hemorrhage
4- myocardial infarction
5- arrhythmia and seizures
6- metabolic acidosis
7- rhabdomyolysis,and hyperthermia
8- Cocaine withdrawal results in depression
Treatment:
1- Benzodiazepines such as diazepam are used to control acute agitation

2- alpha/beta agents such as labetalol or alpha – blockers such as phentolamine for
HTN
Benzodiazepines
- Somnolence, dysarthria, ataxia and stupor

- Flumazenil is the specific antidote
Barbiturates: (Phenobarbital)
Clinical pictures :
1- Respiratory depression
2- CNS depression
3- hypothermia
4- loss of deep tendon reflexes and corneal reflexes
Treatment: urinary excretion by bicarbonate.
Hallucinogens: (Marijuana, LSD, mescaline, peyote,

psilocybin)
Clinical pictures :

267
- delirium and bizarre behavior

- anticholinergic effects, such as flushed skin, dry mouth, dilated pupils, and
urinary retention,
Treatment: benzodiazepines.
HEAVY METALS
Mercury
Source. Thermometers, sphygmomanometers, cathartic medicines, paints, and

cosmetics
- Easily crosses the blood – brain barrier.
Clinical Pictures:
• Pulmonary: interstitial pneumonitis

• Neurologic: tremors, excitability,memory loss, delirium, insomnia collectively
known as “erythrism”
• Gastrointestinal: nausea,vomiting,pain,and bleeding
Treatment
• Removal from source

• Oral chelation with succimer or dimercaprol
Lead
Source: paint, soil, dust, drinking water, gasoline
Metabolism:
- absorbed from GI, skin, inhalation
- Excretion: mainly urine, minimally stool
Clinical pictures:
1- Adult: Abdominal pain, anemia, renal disease, and neurologic manifestations >>
headache and memory loss, Hypertension
2- Children: -Acute: abdominal pain, anemia, lethargy, seizures, and coma
- Chronic: irreversible neurologic damage >>mental retardation and poor cognitive

and behavioral function.
Diagnosis:
268
1- Lead level
2- X ray: lead lines
3- Anemia, Azotemia
Treatment:
- Chronic : According to levels: (EDTA, BAL, Penicillamine, succimer)

• Mild (5−44 mcg/dL): no treatment needed; repeat level in 1 month
• Moderate (45−69 mcg/dL): 2, 3 dimercaptosuccinic acid (DMSA)
• Severe (≥70 mcg/dL): DMSA + EDTA (calcium disodium edentate)
- Acute: Charcoal
LITHIUM
- Used in treatment of bipolar disease
Clinical pictures:
• Acute poisoning:
- GIT: nausea, vomiting, cramping, and possible diarrhea
- CNS: tremulousness, dystonia, hyperreflexia, and ataxia
- ECG: T-wave flattening
• Chronic poisoning:
- altered mental status,coma and seizures
• systemic effects:
- renal: Nephrogenic diabetes insipidus, renal tubular acidosis, tubulointerstitial
nephritis, nephritic syndrome
- Thyroid: hypothyroidism
- Blood: leukocytosis (Acute), Aplastic anemia (chronic)
Diagnosis: high lithium blood level
Treatment:
- Supportive therapy
- Airway protection to prevent aspiration
- BZD, phenobarbital, propofol for seizures
- Gastric lavage within 1 hour of ingestion
- IV hydration
- Hemodlialysis: if renal failure or cannot take IV fluid

269
SALICYLATES
Clinical Pictures:
1- Nausea, vomiting, and gastritis.

2- Tinnitus
3- Hyperthermia
4- confusion,coma, seizures, encephalopathy
5- Metabolic acidosis and high anion gap.
Diagnosis
1- aspirin level: The most specific test

2- High anion gap with metabolic acidosis.
3- high prothrombin
4- hypoglycemia
Treatment:
1- Gastric decontamination
2- Charcoal
3- urinary excretion by alkalization of the urine with IV fluid
4- Dialysis
TRICYCLIC ANTIDEPRESSANTS
Clinical Pictures:
1- Anticholinergic: dry mouth, tachycardia, dilated pupils, and flushed skin.

2- Cardiac dysrhythmia: widening of the QRS complex, ventricular tachycardia,
first – degree conduction blocks status
3- Confusion, seizure.
Diagnosis:
1- Serum drug levels are the most specific test

2- ECG
Treatment:
1- Charcoal
2- Bicarbonate protects the heart form the TCAs

270
ANTICHOLINERGIC POISONING
Anticholinergic effects:
• Diphenhydramine
• Scopolamine and hyoscyamine
• TCAs
• Cyclobenzaprine
• Benztropine
• Benztropine
• Belladonna
Clinical Pictures :
• “Red as a beet”:flushed, red skin due to cutaneous vasodilatation
• “Dry as a bone ” dry skin (anhydrosis) due to inability
• “Hot as a hair” anhydrotic hyperthermia
• “Blind as a bat”:mydriasis
• “Mad as a hatter”: delirium, psychosis, hallucination.
• “Full as a flask”: urinary retention and absent bowel sounds
• Tachycardia
Treatment:
1- ABCs 2- supportive care 3- ECG
4-sodium bicarbonate to stabilize heart 5- Benzodiazepines: seizures
ORGANOPHOSPHATES ‫مبيدات الحشرية‬

- patients will be Farmers or gardeners.
DUMBELSS syndrome:
• Defecation
• Urinary incontinence
• Muscle weakness, miosis
• Bradycardia / bronchospasm
• Emesis
• Lacrimation
• Salivation
• Seizure
Diagnosis: RBC cholinesterase levels.
Treatment:
1- Put on protective clothing

2- remove clothing immediately
3- atropine immediately
4- pralidoxime (2-PAM)

271
ALCOHOL
1- Mild withdrawal:
Tremors, tachycardia m and anxiety
2- Delirium tremens (DT):

• Manifests 48-72 hours after the last drink
but can last up to 10 days
• Mental confusion
• Autonomic hyperactivity
• Visual hallucinations
• Severe agitation
• Diaphoresis
3- Alcoholic hallucinosis:
• May be confused with DT
• Starts 12 – 24 hours after last drink but can last days to weeks
• Paranoid psychosis
• Normal vital sing
• No agitation
• Normal appearance except for auditory (most common),visual
4- Wernicke encephalopathy:
• Confusion, ataxia and ophthalmoplegia (nystagmus)
5- Korsakoff psychosis
• Amnesia and confabulations
Treatment
1- Benzodiazepines: Diazepam and chloridiazepoxide

2- Hydrate with isotonic fluids
3- electrolyte replacement

272

273
SUBARACHNOID HEMORRHAGE
Definition: the sudden onset of bleeding into the subarachnoid space
Etiology: Aneurysm of circle of Willis (saccular or fusiform):
1- anterior communication
artery
2- middle cerebral artery
3- posterior
communicating artery
Clinical pictures:
1- Sudden onset of severe

headache
2- loss of consciousness
3- compressing of occulomotor cranial (3rd nerve palsy)
4- Nuchal rigidity, photophobia, headache, papilledema, meningeal irritation.
5- Fever
6- Long term complication: focal deficits, seizures, rebleeding hydrocephalus
7- Stroke from Vasospasm after the bleed
8- Rebleeding occurs when the clot falls off
9- Hydrocephalus because blood clog up the arachnoids
Granulations
Diagnosis:
1- CT scan: initial test is

2- lumbar puncture: show red cell or
xanthochromia (4-6 hour)
3- Angiography: is used to determine the
specific anatomic site.
4- ECG: enlarged T- Waves
Treatment:
1- maintaining systolic blood pressure at 110 - 160 mm Hg

2- corticosteroids: prevent hydrocephalus
3- Nimodipine (CCB): that can be used to lower the risk of spasm.
4- Angiography to determine the anatomic site
5- surgical correction (embolization or clipping AVM)
6- shunting if hydrocephalus occur

274

275
Heat Disorders
Types:
1- exertional: heat cramps, heat exhaustion, heat stroke
2- Nonexertional: disorders malignant hyperthermia, neuroleptic malignant
syndrome.
Heat cramps Heat Exhaustion Heat stroke
Severity Mild Moderate Sever

- confusion,
disorientation,
nausea,blurred
Symptoms - painful muscular - Mild neurologic vision,and seizures
contractions symptoms such as - High BUN, Creatinine,
muscle tenderness headache, nausea, WBC
- no neurological and anxiety - Rhabdomyolysis,
symptoms hemoconcentration,
anuria, lactic acidosis,
DIC
Sweating able Able Not able
Temperature normal High Very high > 41
1- oral fluid 1- IV fluid replacement

2- electrolyte 2- rapid cooling of the
1- rest
replacement body
2- oral rehydration
3- intravenous 3- Chlorpromazine,
3- salt replacement
Treatment hydration diazepam for shivering
• Malignant Hyperthermia :
- Acute metabolic condition characertized be extreme heat production
- more common in children
- isolated case or family history ( AD inheritance )
- Anesthetic agents such as halothane or succinylcholine which increase free
intracellular calcium followed by excess Ca binding to skeletal muscles
initiates and maintains contraction that lead to anerobic metabolism ,
metabolic acidosis , lactate accumulation , heat production , and cell
breakdown
- clinical pictures :

276
tachycardia ( earliest sign ) , unstable BP , tachypnea , cyanosis , dark urine ,

trismus , high temprture ( late sign ) high CO2 level , electrolyte imbalance ,
renal failure , cardic failure , DIC ,
- Treatment: dantrolene.
• Neuroleptic Malignant Syndrome.
- Phenothiazines or butyrophenones such as haloperidol.
- Muscular rigidity, rhabdomyolysis
- Treatment: stopping the drug, bromocriptine or dantrolene
Hypothermia
definition :
- reduction of core temperature below 35
- sever hypothermia core temperature below 30
- core temperature is measured by rectal probe or through the esophagus
clinical pictures :
- lethargy, confusion, weakness
- arrhythmia: most common cuase of death
- metabolic acidosis, respiratory acidosis, kidney injuery, hyperkalemia
Diagnosis: ( ECG)
1- ventricular fibrillation/ tachycardia
2- Osborne wave : elevation of J- point
Treatment :
Active external rewarming
1- Only to truncal areas
2- Warm blankets
3- Heat lamps
4- Hot-water bottles
Active internal rewarming

1- Warm IVFs (45° C)
2- Warm humidified oxygen (45° C)
3- Warmed gastric lavage via NGT
4- Warmed hemodialysis

277
VENOMOUS BITES AND STINGS

Cat and Dog Bites
1- Cat bite: pasteurella multocida

2- Dog bites: pasteurella, Eikenella, β hemolytic streptococci, Staph aureus, and
Capnocytophaga canimorsus.
Treatment:
- exploration, debridement, irrigation, and proper wound care
- amoxicillin and clavulanate, moxifloxacin
Indications for antibiotic prophylaxis:
• For any cat bite

• Any bite on hand,face, or genitals
• Immunocompromised patients
• Asplenic patients
Most wounds should be left unsutured except for facial wounds for cosmetic reasons.
Never suture the hand
Human Bites
- Most common anaerobic and aerobic bacteria, Eikenella Corrodes.
- Hepatitis B and HIV can be transmitted
Treatment:
1- Clean and irrigate wound well

2- the bite is <12 hours old, close loosely
3- counseling for tetanus, hepatitis
4- prophylactic antibiotics 5-7 day
Rabies:
Etiology: bite by raccoons, rats, dog, fox
- fatal 100 % once the disease has been contracted
Clinical pictures:
1- incubation period up to 1 year

2- prodrome 2- 10 day: fever, paresthesias at sit of bite
3- neurological: aphasia, paralysis, hypersalivation, myoclonus
Diagnosis: viral culture from saliva, CSF, serum

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Treatment:
1- ribavirin (antiviral): for confirmed cases
2- human rabies immunoglobin (HR 16)
3- human diploid cell vaccine (HDCV)
Guidelines for vaccinations:

• No exposure (for high risk people): 3 doses of vaccine
• Post exposure vaccination: Wound cleaning then:
- If never vaccinated: 4 doses of vaccine (0,3,7,14 day) + rabies immune globulin
- If vaccinated before: 2 doses (0,3 day) + + rabies immune globulin
Snakebites:
- Snake venom contains hemolysis toxin, cardiotoxin, neurotoxin, and proteolytic
enzymes.
Treatment:
1. Immobilize the patient
2. Apply compression bandage
3. Antivenin
4. Supportive: Hypotension is managed with fluids, Ventilatory support may be
necessary
Ineffective therapy: incision and suction of

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Chapter 10
Neurology

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‫‪Chapter 10: Neurology‬‬

‫‪282‬‬
SPINAL CORD COMPRESSION

- Acute syndrome of back pain associated with compression of the spinal cord
Etiology:
1- Acute: trauma
2- Sub acute: most common
Cause-neoplasm
3- Chronic: herniation
Clinical Pictures:
1- Pain: earliest symptoms
2- Mild sensory disturbance
3- lower extremity weakness
4- Sphincter / sexual dysfunction
5- increased lower extremity
muscle tone
6- Upper motor neutron signs
below the level of
compression.
Note: thoracic cord is the most
common site of compression
Diagnosis:
1- Plan x-rays
2- MRI : diagnostic test of
choice
3- CT myelogram: if MRI is
contraindicated
Treatment.
1- High-dose dexamethasone
2- radiation therapy for
radiosensitive tumors
3- Surgical decompression for a herniated disk, epidural abscess, or hematoma.

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SYRINGOMYELIA
- Cavitation of the spinal cord.
Types:
1- Communicating syringomyelia: congenital Arnold Chiari malformation

2- non- communicating : trauma or tumors of
cervical vertebrae
Clinical pictures:
1- Sensory dissociation with impaired pain and

temperature occurs in a cape-like distribution
across the neck and arms.
2- Sparing of tactile sensation, position, and
vibratory sense.
3- Reflexes are lost.
4- Lower motor neuron manifestations at the
level of the lesion
5- Upper motor neuron signs below the lesion.
6- Most commonly cervical cord.
Diagnosis: MRI is the most accurate diagnostic test.
Treatment: surgical.
SUBACUTE COMBINED DEGENERATION
Etiology: Vitamin B12 deficiency.
Clinical pictures:
1- Distal paresthesias and weakness of the extremities

2- Spastic paresis and ataxia.
3- On exam there is a combined deficit of vibration and proprioception with
pyramidal signs (plantar extension and hyperreflexia).
Diagnosis: Low serum vitamin B12
Treatment: vitamin B12 replacement.

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ANTERIOR SPINAL ARTERY OCCLUSION

- Acute onset of flaccid paralysis >> spastic paresis over days to week.
- Loss of pain and temperature sensation
- sparing of vibration and position sense
- Everything (motor, sensory, autonomic) is lost below the level with the striking
exception of retained vibration and position sense.
- Treatment is supportive.
BROWN-SEQUARD SYNDROME
Hemisection of the cord

Clinical pictures:
Blow the level of the lesion: 2 ipsilateral signs and 1 contralateral sign.
• Ipsilateral spastic paresis
• Ipsilateral loss of joint position sense, tactile discrimination, and vibratory
sensations
• Contralateral loss of pain and temperature sensation starting 1 or 2 segments
below the lesion
At the level of the lesion:
• ipsilateral loss of all sensation, including touch modalities pain and temperature,
• Ipsilateral flaccid paralysis.

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CEREBROVASCULAR ACCIDENT (CVA)

- A sudden onset of a focal
neurologic deficit.
Note: transit ischemic attack (TIA):

temporary stroke <24 hour
Etiology:
1. Large artery thrombosis.

2. Small artery thrombosis (lacunar).
3. Embolic (cardiogenic or artery-to-artery).
4. Vascular dissection.
5. Systemic hypertension.
6. Bleeding.
Clinical pictures:
I- Occlusion of the ACA:

1- contralateral weakness and
sensory loss in the leg more
than in the upper extremity
2- Urinary incontinence
3- Confusion and behavioral
disturbances.
II- Occlusion of the MCA:

1- contralateral hemiplegia
2- contralateral hemisensory
loss
3- homonymous hemianopia
with eyes
deviated toward the cortical
lesion.
4- Aphasia: Dominant
hemisphere.
III- Occlusion of the PCA:

1- contralateral homonymous hemianopia
2- visual hallucinations
3- Agnosias.
4- Weber syndrome
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5- Benedikt syndrome
IV- occlusion of basilar artery

1- Locked syndrome: (paramedian syndrome)
2- Wallenberg syndrome
V - Occlusion major cerebellar arteries

1- vertigo, vomiting
2- nystagmus
3- Ipsilateral limb ataxia.
Diagnosis:
1- Non-contrast CT scan Initial test of choice.

2- Diffusion-weighted MRI is the most accurate test for detecting cerebral ischemia.
3- Diagnostic workup of patients with acute
ischemic stroke (echocardiogram, carotid
duplex, and 24-hour Holter monitor)
4- Workup for inherited hypercoagulability
5- ECG: Subarachnoid hemorrhage
abnormalities >>inverted T-waves, called
cerebral T-waves.
Treatment:
1- Tissue plasminogen activator.

2- Antiplatelet therapy: aspirin and/or dipyridamole, or switch to clopidogrel.
3- Subarachnoid hemorrhage: Nimodipine >>Early surgical intervention to clip off
the aneurysm or embolize the vessel with a catheter.
4- Carotid endarterectomy
5- Carotid angioplasty and stenting

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Sudden weakness (CVA)
CT scan
Bleeding no bleeding
< 3 hours > 3 hour

Nim o d ip in e +
Sy x ( c lip o f f
o r em b o l ize)
TPA Sta rt If on spirin
asp irin
Ad d Sw it ch to
d ip y rid a m o le
clo p id o g r el
SEIZURES AND EPILEPSY
Seizures: Paroxysmal event due to abnormally discharging central nervous system

(CNS) neurons.
Epilepsy: condition of recurrent seizures due to a chronic underlying process.
Etiology. “VITAMINS”.
1- Vascular: bleed, stroke, arteriovenous malformation
2- Infection: meningitis, encephalitis, abscess
3- Trauma / Toxin: cocaine, benzodiazepines, barbiturates, alcohol,
Phencyclidine
4- Autoimmune: vasculitis
5- Metabolic: Hypo >> hypoNa, hypoCa hypoMg, hypoglycemia, hypoxia
6- Idiopathic
7- Neoplasm
8- Psychiatric

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Clinical Pictures:
1- Paroxysmal, involuntary event (associated abnormal movement or change of

consciousness or both)
2- With or without aura
3- Incontinence, tongue biting, headache.
Partial
Discrete portion of brain
Types:
Simple Complex
No loss of Carbamazepi ne Loss of
consciousnes Phenytoin consciousness
s
Generalized
Arise from both cerebral
hemispheres
Grand mal Absence Atonic Myoclonic

- To n ic (petit mal)
co n tr a ct io n o f - Su d d en lo ss o f
- Su d d en - Su d d en b r ief
m u sc le s lo s s o f m u sc le
co n sc io u sn e s s w ith p o stu r al to n e co n tra ct io n
fo llo wed b y lo s s o f p o s tu ra l
in ter m i tten t la st 1 - 2
to n e seco n d s
relax at io n - EEG : g en eral iz ed
sy m m e tr i c 3 - Hz-
sp ik e – an d - wav e
d is ch ar g e
Valproic acid Ethosuximide:

Phenytoin Valproic Valproic
first line
Lamotrigine acid acid
Valproic acid
Carbamazepin
e
Status epilepticus: recurrent or continuous seizures (5-30 min)
Diagnosis:
1- EEG is the test of choice for the diagnosis of epilepsy

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2- serum electrolytes, glucose, toxicology, arterial blood gas

3- CT scan or MRI.
Treatment.
I- Acute:
1- ABC (airway breathing, and circulation)
2- Simultaneously evaluate and treat any precipitating causes of seizure.
3- if continue seizure >> follow the scheme
Sid e ef f e ct :
- lo r az ep am , d ia zep am ( b en zo d ia zep in e s): wo rk o n GA B A re cep t or
- p h en y to in ( in h ib i t s N a act io n p o t en t ia ls) : d ip l o p ia, d izz in e s s, a tax ia,
g u m h y p er p l as ia, ly m p h ad en o p ath y , h ir su ti sm , r ash
- Ph en o b ar b i tal : sed at io n , atax ia, ra sh
- Lam o t r ig in e ( d e cr e as e g lu tam at e re lea se) : St ev en s – Jo h n so n sy n d ro m e

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Notes:
1- anticonvulsant therapy indication:
- abnormal neurologic Ex
- status epilepticus
- strong family history of seizures
- abnormal EEG
2- first time seizure NOT treated with long term anticonvulsant therapy
3- stop anticonvulsants if pt free of seizure 2-3 years
4- sleep deprivation EEG determine if pt at low risk of recurrence
VERTIGO AND DIZZINES

- False sensation of movement.
Etiology: Meniere, labyrinthitis, positional vertigo, traumatic vertigo, perilymphatic

fistula, cervical vertigo, vascular disease of the brain stem, arteriovenous
malformations, brain tumor, multiple sclerosis, drug overdose, vertebrobasilar
migraine.
Clinical Pictures:
1- Sensation of movement without actually moving environment spinning around

them.
2- Tilting, swaying, failing forward or backward
3- nausea, vomiting

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Presyncope Vertigo
Light headiness Spinning around
Weakness Tilting
Palpitates Swaying
SOB Falling
CVS CNS
Meniere disease:
- tinnitus, hearing loss, and episodic vertigo (1 to 8 hours)
- wax and wane
- Most common causes: syphilis and head trauma.
Benign paroxysmal positional:
- Exacerbated by head movement or change in head position.
- Latency of several seconds after head movement before
- Last 10 to 60 seconds.
Labyrinthitis:
- severe vertigo that lasts for several days with hearing loss and tinnitus
- Follows an upper respiratory tract infection.
Preilymphatic fistula:
Head trauma, extreme barotrauma during air flight, scuba diving, or vigorous
Valsalva maneuver, Explosions deafen people.
Central vertigo:
Cerebellar or brain-stem tumor, bleed, ischemia, Toxicity or overdoses, multiple
sclerosis.
Treatment:
- Meclizine, diazepam.
- Meniere disease: low-salt diet and diuretic >> if fail >>Surgical decompression.
- Benign paroxysmal positional vertigo: positional maneuvers move otolith out of
the circular canals.
- Vertigo labyrinthitis: Meclizine, diazepam, Steroids.

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HEADACHE
Pain located in the head, neck, or jaw.
Etiology:
1- Primary migraine, cluster, and tension.

2- Secondary intracranial hemorrhage, brain tumor, meningitis, temporal arteritis,
and glaucoma.
Clinical pictures:
1- Meningitis: Headache with fever and nuchal rigidity

2- intracranial hemorrhage: “worst headache of my life” and/or “thunderclap”
+nuchal rigidity without fever
3- Brain tumors: deep, dull, aching pain that disturbs deep.
4- posterior fossa brain tumors: Headache induced by coughing lifting, or bending
5- Patients temporal arteritis: unilateral pounding headache associated with visual
changes, polymyalgia rheumatic, jaw claudication, fever, weight loss, and scalp
tenderness, age>50.
6- Migraine:
- recurrent syndrome of headache, nausea/ vomiting,
- pulsatile, throbbing, unilateral, and aggravated by minor movement
- photophobia, phonophobia
- Triggers: alcohol, certain foods (such as chocolate, various cheeses,
monosodium glutamate), hunger, irregular sleep patterns.
• Migraine without aura is a migraine without a preceding focal neurologic deficit.
• Migraine with aura (classic migraine): aura consists of motor, sensory, or visual
symptoms (starts, sparks, and flashes of light).
• Complicated migraine >> neurologic deficits after pain resolution
• Basilar migraine. >> Symptoms of brain stem (vertigo, diplopia, ataxia...)
7- Tension headaches: tight, bank-like headaches that occur bilaterally+ Tightness
of the posterior neck muscles.
8- Cluster headaches:
- unilateral, periorbital, and peaking in intensity within 5 minutes of onset
- Rhinorrhea, reddening of the eye, lacrimation, nasal stuffiness, nausea, and
sensitivity to alcohol.
Diagnosis: CT scan of the head to rule out any secondary causes.

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Treatment:
1- Modify lifestyle by avoiding those triggers.

2- Treatment of migraine
- Triptans contraindicated in:CVS diseases, uncontrolled HTN, pregnancy

- Opioid not routinely used (because of possibility for addiction) >> only for
severe cases
3- Treatment of tension headaches: relaxation activities, acetaminophen NSAIDs,
muscle relaxant.
4- Cluster headaches:
- a triptan
- 100% oxygen
- Calcium channel blocker
- Prednisone and lithium
PSEUDOTUMOR CEREBRI
- Idiopathic increase in intracranial pressure
Etiology:
- More common in women obesity, chronic lung disease, Addison disease, oral
contraceptives, tetracycline use, and vitamin A toxicity.
Clinical pictures:
- Headache
- visual disturbances as diplopia
- Sixth cranial nerve (abducens) palsy.
- Diplopia, papilledema, enlargement of the blind spot on visual field testing.
- CT and MRI are normal.

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Treatment:
1- Weight loss
2- removing offending agents such OCP
3- Diuretics: acetazolamide, furosemide
4- Steroids: prednisone
5- repeated lumbar punctures
6- Surgical shunt.
TRIGEMINAL NEURALGIA
- Idiopathic pain syndrome resulting in sudden, severe, sharp pain starting near the
side of the mouth and progressing to the ear, eye, or nostril.
- Triggered by touching, talking, eating.
- Treated: carbamazepine (first choice)>>if fail >> phenytoin, baclofen,
gabapentin >> if fail >>surgery, radio-frequency.
GUILLAIN-BARRE SYNDROME (GBS)

- Autoimmune destruction myelin.
Etiology. Misdirection of the immune

response.
Clinical pictures:
1- Rapidly developing weakness that

typically
begins in the lower extremities and moves
upward.
2- Lack reflexes in the muscle groups.
3- Fever, constitutional symptoms, or
bladder dysfunction are rare
4- sensory disturbances pain or tingling
dysesthesia.
5- Autonomic instability (profuse sweating, postural hypotension, labile blood
pressure, cardiac dysrhythmias)
6- History of an infection GIT or respiratory (Campylobacter jejuni).
Diagnosis:
1- Lumbar puncture: initial test >> high protein without cell

2- electromyography (EMG):most accurate test

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Treatment: Intravenous immunoglobulin and plasmapheresis
MYASTHENIA GRAVIS
Etiology: Autoimmune process
characterized by acetylcholine-
receptor antibodies.
Clinical Pictures:
1- Muscle weakness and

fatigability.
2- Diplopia, ptosis, and difficulty
swallowing.
3- Speech is “mushy” or nasal
quality
4- “Snarling” appearance when smiling.
Eaton-lambert myasthenic syndrome :
- Antibodies against Ca+2 channels in the presynaptic nerve

- Commonly with Small -cell carcinoma of the lung
- Clinical pictures: proximal muscle weakness, hyporeflexia
- Don’t affect eye muscles and no fatiguability (improve with
movement)
- Diagnosis: EMG>> increasing muscle strength on repetitive
stimulation
- Treatment: treat lung cancer, IVIG, cortisone
Diagnosis:
1- acetylcholine-receptor antibody test: Best initial test

2- Edrophonium (Tensilon) test
3- chest X-rays and CT for thymoma
4- electromyography (EMG): most accurate

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Treatment:
Anticholinesterase (pyridostgimen or neostigmine)
Fails
Thymectomy
Fails
Steroid 1-3 months
Fails
Immunosuppressive therapy (azathioprine) 3-6 months
Notes:
1- Plasmapheresis and intravenous immunoglobulin acute myasthenic crisis.

2- Aminoglycoside should be avoided.
3- Mycophenolate is newer immunosuppressive drug less side effect
AMYOTROPHIC LATERAL SCLEROSIS

- Idiopathic disorder of both upper and lower motor neurons.
Clinical pictures:
1- Muscle weakness combined

2- Signs of upper motor neuron loss:
weakness
with spasticity and hyperreflexia.
3- cranial nerve palsies
4- respiratory involvement
5- lower motor neuron destruction:
weakness with
muscle wasting, atrophy, and fasciculation’s
Diagnosis:

297
1- electromyogram:most accurate
2- CPK: mildly elevated
3- CSF, MRI normal
Treatment:
1- Riluzole: inhibits glutamate

release
2- Spasticity is treated with baclofen
and tizanidine.
Upper motor neuron lesion Lower motor neuron lesion

Hyperreflexia Hyporeflexia or areflexia
Hypertonia Hypotonia or atonia
Rigidity and spacticity Flaccidity
Weakness with no or little muscle atrophy Weakness with sever muscle atrophy
No fasciculation or fibrillation Fasciculation and fibrillation of muscle
Positive plantar reflex (babinisci) No plantar reflex
1- Primary lateral sclerosis 1- Poliomyelitis
2- Hereditary spastic paraplegia 2- Spinal muscular atrophy
3- Adreno-myeloneuropathy 3- Primary muscular atrophy
4- HIV associated myelopathy 4- Benign focal amyotrophy
5- Amyotrophic lateral sclerosis 5- Amyotrophic lateral sclerosis

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MULTIPLE SCLEROSIS
Autoimmune inflammatory disease of CNS white matter
Etiology:
- Multifactorial >> Genetic +environment

- Characterized by focal areas of demyelination.
Clinical pictures:
1- Weakness, numbness, tingling or

unsteadiness of a limb.
2- Urinary urgency or retention,
3- Blurry vision, double vision.
Forms of the disease.
• Relapsing remitting disease.

• Secondary progressive disease.
• Primary progressive disease.
Diagnosis:
1- MRI >> Increased T2 and decreased T1 intensity represent.

2- Evoked response potentials >>slow response to stimuli
3- CSF >> oligoclonal bands

299
Treatment: is divided for:
1- Disease –modifying therapy

- Replacing-remitting
disease:
• Interferon- β1a
• Interferon- β1b
• Glatiramer acetate
- Secondary progressive
disease:
• IFN- β1b
• Mitoxantrone: used in
normal ejection fraction
because of dose-related
cardiotoxicity
• Methotrexate, cyclophosphamide, IV immunoglobulin, azathioprine
- Primary progressive disease.
• No approved disease-modifying therapy exists at this time
Notes:
1- Fingolimod: disease-modifying medication>> decrease progression

2- Dalfampridine: disease-modifying medication >> increases walking speed.
2- Treatment of acute exacerbation :
- IV steroid for 3 days then oral taper over 4 weeks
- If unresponsive to steroid >> plasma exchange
3- Treatment of complication
- Spasticity: baclofen.
- nocturnal spasticity: Tizanidine and diazepam
- Trigeminal neuralgia: carbamazepine, gabapentin, phenytoin, pregabalin, TAC.
- Bladder hyperactivity: oxybutynin
- Urinary retention: bethanechol.
- Fatigue: amantadine or fluoxetine.
- Erectile dysfunction: sildenafil acetate.

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HUNTINGTON DISEASE
- Genetic degenerative brain disorder.
Etiology:
- Gene located on chromosome 4p.

- Gene contains CAG trinucleotide repeat expansion that codes for a protein called
huntingtin.
Clinical pictures:
1- Chorea and behavioral disturbance.

2- Choreic gait
3- Irritability, anger, paranoia, or signs of depression.
4- Lack of judgment, disinhibition, and inattention.
Diagnosis:
1- Genetically testing for the presence of the CAG trinucleotide.

2- CT: cerebral atrophy.
Treatment:
1- Tetrabenazine: for movement disorder.

2- Haloperidol or clozapine: for behavioral changes.
PARKINSON DISEASE
- Neurologic syndrome resulting from the deficiency of the neurotransmitter
dopamine.
Etiology:
1- Drugs: haloperidol, chlorpromazine, metoclopramide, alpha-methyldopa, and

reserpine.
2- Toxin: MPTP, carbon monoxide, cyanide,
3- trauma, tumor, abscess, infract
4- Post encephalitic Parkinsonism.
Clinical pictures: British gentleman.
1- Bradykinesia
2- Rigidity (cogwheel)

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3- Instability (postural)
4- Tremor (resting)
5- “Parkinson plus” syndromes.
• Parkinsonism + vertical gaze palsy =
supranuclear palsy
• Parkinsonism + prominent ataxia =
olivopontocerebellar atrophy
• Parkinsonism + prominent orthostatic
hypotension – Shy-Drager syndrome (now called
multiple-system atrophy)
Treatment:
Dopamine agonist Anticholinergics
1- Carbidopa /levodopa 1- Benztropine
2- COMT inhibitors 2- Trihexyphenidyl
3- Selegiline
4- Amantadine
5- Pramipexole
6- Ropinirole
7- Bromocriptine
8- Cabergoline
Depend on patient's functional status:
Intact functional status
< 60 years > 60 years
Benztropine Amantadine

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Compromised functional status
<60 years > 60 years
Carbidopa /levodopa Pramipexole / Ropinirole

Side effect: Low potency
1. Dyskinesia
2. Akathisia
3. No – off phenomena
1- Using sustained release Carbidopa/levodopa -add Selegiline

2- add Selegiline
3- add dopamine agonist
4- add COMT inhibitor
5- restrict protein meal at night
- surgery: pallidotomy or thalamotomy (last resort)
BENIGN ESSENTIAL TREMOR
- Idiopathic disorder consisting of an isolated tremor of the hands, head or both.

- Worsened by the use of caffeine or beta agonists.
- Improvement with the use of alcohol.
- Treatment is Propranolol >> if fail >> primidone, alprazolam, clozapine >> if fail
>> thalamotomy
RESTLESS LEG SYNDROME
- Idiopathic condition resulting in a sensation of creeping crawling dysesthesia

within the legs
- Leading to involuntary movements during sleep.
- Exacerbated by sleep deprivation, caffeine, and pregnancy.
- No specific diagnosis test for this disorder.
- Treatment is a dopamine agonist such pramipexole or ropinirole.

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DEMENTIA
- slight (mild) or prominent (severe) memory disturbances coupled with other

cognitive disturbances that are present even in the absence of delirium
Etiolgy:
1- Neurodegenerative disease: Alzheimer, Parkinson, Huntington, Pick, fronto-

temporal degeneration, and Creutzfeldt-Jakob disease
2- Cerebrovascular disease:CNS infections (e.g., HIV), traumatic brain injuries,
radiation, and/or tumors.
3- Seizure disorders
4- metabolic disorders: disease of protein, lipid, and carbohydrate metabolism
5- diseases of myelin: Wilson disease, uremic encephalopathy
6- endocrinopathies: hypothyroidism.
7- Nutritional deficiencies: beriberi (thiamine [vitamin B1] deficiency), pellagra
(niacin deficiency), and/or pernicious anemia (cobalamin [vitamin B12] deficiency),
8- Toxins: alcohol, inhalants, sedative–hypnotics, anxiolytics, anticonvulsants,
antineoplastic medications, heavy metals, insecticides, solvents.
Specific dementias:
1- Dementia due to Alzheimer disease

• Found in 50–60% of patients with dementia (most common cause)
• Risk factors: Female, family history, head trauma, Down syndrome
• Neuroanatomic findings: Cortical atrophy, flattened sulci, and enlarged ventricles
• Histopathology: Senile plaques (amyloid deposits), neurofibrillary tangles, neuronal
loss, synaptic loss, and granulovacuolar degeneration of neurons
• Associated with chromosome #21 (gene for the amyloid precursor protein)
• Decreased Ach and NE
• Deterioration is generally gradual; average duration from onset to death is ~8 years.
• Focal neurologic symptoms are rare.
• Treatment includes long-acting cholinesterase inhibitors such as donepezil,
rivastigmine, galantamine, and memantine..
2- Vascular dementia (multi-infarct dementia)

• Risk factors: Male, advanced age, hypertension, or other cardiovascular disorders
• Affects small and medium-sized vessels
• Examination may reveal carotid bruits, fundoscopic abnormalities, and enlarged
cardiac chambers.
• MRI may reveal hyperintensities and focal atrophy suggestive of old infarctions.
• Deterioration may be stepwise or gradual, depending on underlying pathology.
• Focal neurologic symptoms (pseudobulbar palsy, dysarthria, and dysphagia are most
common)
304
• Abnormal reflexes and gait disturbance are often present.

• Treatment is directed toward the underlying condition and lessening cell damage.
• Control of risk factors such as hypertension, smoking, diabetes,
hypercholesterolemia, and hyperlipidemia is useful.
3- Pick disease
• Neuroanatomic findings: Atrophy in the frontal and temporal lobes
• Histopathology: Pick bodies (intraneuronal argentophilic inclusions) and Pick cells
(swollen neurons) in affected areas of the brain
• Etiology is unknown.
• Most common in men with family history of Pick disease
• Difficult to distinguish from Alzheimer’s
• May see features of Klüver-Bucy syndrome (hypersexuality, hyperphagia, passivity)
4- Creutzfeldt –jakob disease
• Rare spongiform encephalopathy is caused by a slow virus (prion).
• Presents with neurocognitive disorder, myoclonus, and EEG abnormalities (e.g.,
sharp, triphasic, synchronous discharges and, later, periodic discharges)
• Symptoms progress over months from vague malaise and personality changes to
dementia and death.
• Findings include visual and gait disturbances, choreoathetosis or other abnormal
movements, and myoclonus.
• Other prions that cause neurocognitive disorder (e.g., Kuru) may exist.
5- Huntington disease
• A rare, progressive neurodegenerative disease that involves loss of GABA- ergic
neurons of the basal ganglia, manifested by choreoathetosis, dementia, and psychosis.
• Caused by a defect in an autosomal dominant gene located on chromosome 4
• Atrophy of the caudate nucleus, with resultant ventricular enlargement, is common.
• Clinical onset usually occurs at approximately age 40.
• Suicidal behavior is fairly common.
6- Parkinson disease
• Common, progressive, neurodegenerative disease involving loss of dopaminergic
neurons in the substantia nigra
• Clinical onset is usually age 50–65.
• Motor symptoms: resting tremor, rigidity, bradykinesia, and gait disturbances.
• dementia occurs in 40% of cases, and depressive symptoms are common.
• Destruction of dopaminergic neurons in the substantia nigra is a key pathogenic
component and may be caused by multiple factors, including environmental toxins,
infection, genetic predisposition, and aging.
• Treatment of Parkinson disease involves use of dopamine precursors (e.g., levodopa,
carbidopa), dopamine agonists (bromocriptine), anticholinergic medications
(benztropine, trihexyphenidyl), amantadine, and selegiline.
• Antiparkinsonian medications can produce personality changes, cognitive changes,
and psychotic symptoms.

305
7- Lewy bodies disease

• Hallucinations, parkinsonian features, and extrapyramidal signs.
• Antipsychotic medications may worsen behavior.
• Patients typically have fluctuating cognition, as well as REM sleep behavior
disorder.
8- HIV related dementia
• HIV directly and progressively destroys brain parenchyma.
• Becomes clinically apparent in at least 30% of individuals with AIDS, beginning
with
subtle personality changes.
• Diffuse and rapid multifocal destruction of brain structures occurs, and delirium is
often present.
• Motor findings include gait disturbance, hypertonia and hyperreflexia, pathologic
reflexes (e.g., frontal release signs), and oculomotor deficits.
• Mood disturbances in individuals with HIV infection are apathy, emotional liability,
or behavioral disinhibition.
9- Wilson disease
• Ceruloplasmin deficiency
• Hepatolenticular degeneration
• Kayser-Fleischer rings in the eye
• Asterixis
10- Normal pressure hydrocephalus
• Enlarged ventricles
• Normal pressure
• dementia, urinary incontinence, and gait apraxia
• Treatment includes shunt placement
11- Pseudodementia
• Typically seen in elderly patient who has a depressive disorder but appears to have
symptoms of neurocognitive disorder; should improve after being treated with
antidepressants
• Can usually date the onset of their symptoms

306
Amnesia
Definition: prominent memory impairment in the absence of disturbances in level of
alertness or the other cognitive problems that are present with delirium or dementia.
Etiology (General Medical Conditions):
1- Commonly associated with bilateral damage to diencephalic and mediotemporal

structures (e.g., mammillary bodies, fornix, hippocampus).
2- head trauma
3- cerebrovascular disease
4- Hypoxia
5- local infection (e.g., herpes encephalitis)
6- ablative surgical procedures, seizures.
7- thiamine deficiency associated with alcohol dependence

307
CRANIAL NERVES
Nerve Name Function Palsy symptoms
I Olfactory Smell Anosmia
II Optic Vision Blindness
III Occulomotor Superior rectus, inferior Diplopia, ptosis,
rectus, medial rectus, inferior mydriasis, strabismus, loss
oblique, levator palpebrae, of upward and medial eye
parasympathetic to pupil, movement
upper eyelid movement
IV Trochlear Superior oblique Loss of down gaze
V Trigeminal Sensation of the face and
mastication of muscle
VI Abducent Lateral rectus Loss of lateral eye
movement
VII Facial Facial muscles, taste Bells palsy: facial
sensations from anterior 2/3 of weakness on same side
tongue, supply all salivary
gland except parotid
VIII Vestibulocochlear Hearing and balance Deafness, nystagmus
IX Glossopharyngeal Sensations of posterior 1/3 of
tongue, supply parotid gland
X Vagus Supply parasympathetic to According to site
body
XI Accessory Supply trabezius, Ipsilateral loss of shoulder
sternocleidomastoid elevation and head tilting
XII Hypoglossal Motor innervations of tongue Tongue deviation to
ipsilateral side of injury
Notes:
1- 3 rd nerve palsy causes:
- Medical causes: DM, HTN >> pupil is reactive
- Surgical causes: aneurysm, hematoma, trauma, tumor >>dilated pupil
2- Abducent nerve is the most common nerve affected in high ICP

308
The Most common
The Most Common

309
‫‪The Most common‬‬

‫‪310‬‬
The Most common
Endocrinology
1. M.C. Pituitary Mass: Prolactinoma
2. M.C.C of SIADH: Small Cell CA of the Lung
3. M.C.C of Death in DKA: Cerebral Edema

4. M.C.C of Peripheral Neuropathy: DM
5. M.C.C Blindness is: Diabetic Retinopathy
6. M.C.C of Charcot joints: Diabetes mellitus
7. M.C.C of Hyperthyroidism: Graves Disease

8. M.C.C of Hypothyroidism in developed countries (JORDAN): Hashimoto’s
Thyroditis
9. M.C.C of Hypothyroidism worldwide: Iodine deficiency
10. M.C Thyroid disease: Goiter
11. M.C.C of Hyperparathyroidism: Adenoma > Hyperplasia > CA

12. M.C.C Cause of secondary Hyperparathyroidism: CRF
13. M.C.C of Hypercalcemia: Hyperparathyroidism / Hypocalcemia
(hypoparathyroidism)
14. M.C.C of Congenital Adrenal Hyperplasia: 21 hydroxylase def.

15. M.C.C of Cushing Syndrome : Exogenous Steroid Therapy
16. M.C.C of Cushing's disease: pituitary microadenoma
17. M.C aldosterone producing adrenal tumor: u/l adrenal adenoma

18. M.C.C of Addison’s Disease : adrenal insufficiency (autoimmune adrenalitis)
Rheumatology
1. M.C. cardiac manifestation of Systemic Lupus Erythematous: Pericarditis
2. M.C.C of Death in SLE pts. : Lupus Nephropathy Type 4 - Diffuse Proliferating
3. M.C. affected joint in gout: First MTP
4. M.C. form of systemic vasculitis in adults: Giant cell (temporal) arteritis
5. M.C joint involved in Osteoarthritis : Knee joint
Gastroenterology
1. M.C.C of infectious esophagitis : Candida Esophagitis
2. M.C.C of Protozoal Diarrhea: Giardia
3. M.C.C of Portal HTN: Liver Cirrhosis
4. M.C.C Liver Cirrhosis in Western communities: Alcohol

311
The Most common
5. M.C.C Liver Cirrhosis in Jordan : Hepatitis B

6. M.C.C of toxic mega colon: Pseudomembranous colitis
Cardiology
1. M.C.C of Death worldwide: Ischemic Heart Dis.
2. M.C site of Atherosclerosis: Carotid Bifurcation
3. M.C.C of Coronary Art. Thrombosis : Left Ant. Descending Art
4. M.C.C Silent Asymptomatic MI: DM
5. M.C.C Rt.-sided heart failure: Lt.-sided heart failure (either systolic or diastolic
heart failure)
6. M.C. for pulmonary edema: Left-sided heart disease
7. M.C. Heart valve involved in RF: Mitral Valve
8. M.C.C of Heart Murmur: Mitral valve Prolapse
9. M.C.C of tricuspid stenosis: Rheumatic heart disease
10. M.C.C of sudden cardiac death among young people: Hypertrophic
Cardiomyopathy (HCM)
11. M.C. form of hypertrophic cardiomyopathy: Asymmetric involvement of the
interventricular septum
12. M.C. primary cardiac tumors in adults: Myxomas
13. M.C site for cardiac myxoma : Left atrium
14. M.C aortic branch involved in Takayasu arteritis: Left subclavian
15. M.C benign cardiac rhythm abnormality: PAC
16. M.C cause of restrictive cardiomyopathy: Amyloid
Hematology
1. M.C.C of Dietary deficiency : Iron
2. M.C Type of Hodgkin’s Lymphoma Mixed Cellularity & Best Prognosis is :
Lymphatic Predominant
3. M.C Type of Non-Hodgkin’s Lymphoma: B-cell lymphomas
4. M.C.C of Hereditary Bleeding Disorders : vWD
5. M.C. Protein in Urine with Multiple Myeloma: Bence Jones Protein
6. M.C.C of hereditary thrombophilia: factor V Leiden mutation
7. M.C hereditary cause of venous thrombosis:factor V Leiden mutation
8. M.C hereditary blood coagulation disorder: factor V Leiden mutation
Infectious Disease
1. M.C.C of Opportunistic infection in AIDS: Pneumocystis Carinii Pneumonia

312
The Most common
2. M.C.C of Myocarditis : Coxsackie A virus

3. M.C.C of Liver Infection: Hepatitis A
4. M.C.C of Acute Infective Endocarditis : Staph Aureus
5. M.C.C of Subacute Acute Infective Endocarditis: Staph Viridans
6. M.C. Heart valve Involved in Bacterial Endocarditis: Mitral Valve
7. M.C. Heart valve Involved in Bacterial Endocarditis in IV drug users: Tricuspid
valve
8. M.C.C of Nosocomial Pneumonia: Staph. Aureus
9. M.C.C of Pneumonia in IV drug Abuser: Staph. Aureus
10. M.C.C of Community Acquired Pneumonia: Strept. Pneumonia
11. M.C.C of interstitial/atypical pneumonia: Mycoplasma
12. M.C.C of bronchopneumonia: Staphylococcal

13. M.C.C of Atypical Pneumonia: Mycoplasma
14. M.C.C of Nosocomial Infection : UTI
15. M.C extra pulmonary site of tuberculosis: Urinary tract
16. M.C cause of fungal infection in AIDS patients: Cryptococcosis
17. M.C. affected bowel segment in TB: Ileocecal area
18. M.C. bacterial cause of mesenteric adenitis : Yersinia Enterocolitica
19. M.C. Causative organism of acute pyogenic meningitis in adults: Strep.
Pneumonia
20. M.C.C of Sepsis in IV drug abuser: Staph. Aureus
21. M.C. etiology for Osteomyelitis: Staphylococcus aureus
22. M.C.C Bacterial Arthritis in Young age: Neisseria Gonorrhea
23. M.C.C of Death in Tetanus: Respiratory arrest
Nephrology
1. M.C.C of Acute RF: Pre-Renal Causes
2. M.C.C of Chronic RF: Diabetic Nephropathy
3. M.C.C of Intrinsic RF : Acute Tubular Necrosis
4. M.C.C of Nephrotic Syndrome in Adults - Focal segmental glomerulosclerosis

5. M.C.C of Nephrotic Syndrome in children: Minimal Change Dis.
6. M.C.C of Glomerulonephritis in Adult: IgA Nephropathy (Berger’s Dis)

7. M.C chronic glomerular disease worldwide: IgA Nephropathy (Berger disease)
8. M.C.C of HTN is: Essential HTN
9. M.C.C of HTN in Young women : OCPs
10. M.C.C of secondary HTN is: Renal disease
11. M.C.C of Death in HTN pts.: Acute MI
12. M.C.C of Nephrocalcinosis in adults: Primary hyperparathyroidism

313
The Most common
13. M.C hereditary human kidney disease - POLYCYSTIC KIDNEY DISEASE

Autosomal-Dominant Type (Adults)
14. M.C.C of renal artery stenosis
- Old age: atherosclerosis
- Young(India): takayasu arteritis
- Young(western world): fibro muscular dysplasia)
15. M.C.C of End Stage Kidney Disease : DM
Pulmonology
1. M.C.C of 2ry Pulmonary HTN: COPD
2. M.C. form of emphysema in smokers: Centrilobular emphysema
3. M.C chest x-ray abnormality in the ICU: Atelectasis
4. M.C location to see Asbestosis sequelae: Posterior lower lobes
Neurology
1. M.C.C of Dementia : Alzheimer's Disease
2. M.C.C of Death in Alzheimer’s pts.: Aspiration Pneumonia
3. M.C.C of Death in Stroke pts.: Aspiration Pneumonia
4. M.C. primary brain tumor: GBM
5. M.C cause of facial hemipalsy: Bell palsy

314
The Most common
Normal Values

315
‫‪The Most common‬‬

‫‪316‬‬
Normal Values
- Sodium ( Na ) : 135-145 mEq/ L

- Potassium (K) : 3.5-5.3 mEq/ L
- Chloride (Cl) : 95-105 mEq/ L
- Calcium ( Ca ) : 8.5 -10.5 mg/dL
- Phosphor ( Po4 ) : 2.5- 4.5 mg/dL
- Magnesium (Mg) : 1.8 – 3 mg/dL
- Serum osmolality : 285-295 mOsm/kg
- Urine osmolality : 38 – 1400 mOsm/kg
- potenz Hydrogen ( ph ) : 7.35 – 7.45
- partial pressure of carbon dioxide (PaCo2) : 35-45 mmHg
- partial pressure of oxygen ( PaO2 ) : 70-100 mmHG
- oxygen saturation of arterial blood ( SaO2 ) : 93% - 98%
- Bicarbonate ( HCO3 ) : 22-26 mmol/ L
- Creatinine ( Cr) : 0.7 -1.4 mg/dL
- Blood urea nitrogen ( BUN ): 7-20 mg /dL
- Total protein : 6-8 g/dL
- Albumin :3.5 – 5 g/dL
- Alkaline phosphates (ALP) : 20-140 IU/L
- alanine aminotransferase (ALT) : 5-35 IU/L
- aspartate aminotransferase (AST) : 5-40 IU/L
- Gamma-glutamyl transferase (GGT) : 0-30 IU/L
- Total bilirubin : 0.2 -1.2 mg/dL
- Direct bilirubin : 0.1 -0.3 mg /dL
- Indirect bilirubin : 0.2 – 0.7 mg /dL
- prothrombin time ( PT ) : 10-12 second
- Partial prothrombin time (PPT ) : 35-40 second
- international normalized ratio (INR ) : 1-2
- Jugular venous pressure (JVP ) : 3-4 cm from sterna angle add 5 cm to calculate
from right atrium
- Liver span :
6-12 cm in right midclavicular line
4-8 cm in midsternal line

317
Normal Values
- Red blood cell (RBC ) :

male 4.32-5.72 million cells/mcL
female : 3.90-5.03 million cells/mcL
- Hemoglobin ( Hb /Hgb ) :
Male: 13.5-17.5 grams/dL :
Female: 12.0-15.5 grams/dL
- Hematocrit (Ht ) / packed cell volume (PCV ):
Male: 38.8-50.0%
Female: 34.9-44.5 %
- White blood cell count ( WBC ) : 3,500 to 10,500 cells/mcL
neutrophils : 54-62 %
band cells : 3-5 %
eosinophils : 1-3 %
basophils : 0-0.75 %
lymphocytes : 25-33 %
monocytes : 3-7 %
- Platelet : 150,000 to 450,000/mcL

318

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C

Abu Gharbieh's Capsule

‫‪Abu Gharbieh, Yazan A.Hashem‬‬

‫‪Abu Gharbieh's Capsule Internal Medicine /‬‬

‫جميع حقوق التأليف والطبع والنشر محفوظة‬

I am glad to offer my expertise and knowledge that I had

1) Kaplan STEP 2 CK Leture Notes

2) Davidson’s Essential of Medicine

Yazan Abu Gharbieh

1) Kaplan STEP 2 CK Leture Notes

2) Davidson’s Essential of Medicine

‫يزن ابو غربية‬

Chapter 6: Infectious Disease

Chapter 9: Emergency Medicine

Chapter 10: Neurology

The Most common

1- Pituitary is surrounded by sphenoid bone

DISEASES OF THE ANTERIOR PITUITARY

1- physiological : Pregnancy, early nursing, sleeps, exercise, Hypoglycemia,

0795407665 ‫الدكتور يزن ابو غربيه‬

1- Women: galactorrhea, menstrual abnormalities amenorrhea, oligomenorrhea,

2- Men: hypogonadism, erectile dysfunction, decrease libido, gynecomostia,

Diagnosis: 1- Pregnancy test 2- Check medications 3- TFT 4- KFT 5- LFT 6-

1- dopamine agonist: bromocriptine, cabergoline

In children called gigantism.

Etiology: 1- Macroadenomas : most common cause

1- Skeletal soft tissue changes.

0795407665 ‫الدكتور يزن ابو غربيه‬

Complications: Heart Failure (most common of Death)

DM, cord compression, visual field defects.

- Partial or complete loss of anterior pituitary

- First hormone to be lost FSH, LH, GH > TSH > ACTH

0795407665 ‫الدكتور يزن ابو غربيه‬

4- ACTH: 2ND Adrenal insufficiency

Empty sella syndrome (ESS)

- herniation of supracellar subarachnoid space through incomplete diaphragm

DISEASES OF THE POSTERIOR PITUITARY.

0795407665 ‫الدكتور يزن ابو غربيه‬

1- hormone Replacement vasopressin, desmopressin

Syndrome of Inappropriate secretion of ADH

Diagnosis: 1- Hyponotremia < 130𝑚𝐸𝑞/ 𝐿 2-Posm < 276 𝑚𝑜𝑠𝑚/𝑘𝑔

0795407665 ‫الدكتور يزن ابو غربيه‬

0795407665 ‫الدكتور يزن ابو غربيه‬

Laboratory test in thyroid:

1- Drug: amiodarone, alpha interferon, lithium, contrast agents

3- Toxic nodule: can result from plummer

1- TSH: low in primary … high in secondary

3- RIAU increase in graves

- endocrine emergency: (extreme thyrotoxicosis)

- Etiology: stress, infection, surgery, trauma

Clinical picture: irritability, delirium, coma, tachycardia, restlessness, vomiting,

0795407665 ‫الدكتور يزن ابو غربيه‬

2- adult: lethargy, constipation, cold intolerance, stiffness & cramping of muscles,

Carpal tunnel syndrome: compression

1- Idiopathic: most common cause

0795407665 ‫الدكتور يزن ابو غربيه‬

1- levothyroxine (T4):Should be monitored TSH/ T3 (it takes 6 weeks to stabilize.

Etiology: Long standing hypothyroidism with precipitating factor

- Cold exposure, trauma, infections, CNS depressants.

Clinical pictures: hypothermic, stuporous state, respiratory depression

Treatment: High dose T4, T3

Etiology: Viral origin follows upper respiratory Infection.

Treatment: NSAID, Prednisone, propranolol

Etiology: autoimmune factor with lymphocytic infiltration.

Abu Gharbieh's Capsule Lecture Notes in Medicine

Abu Gharbieh's Capsule Lecture Notes in Medicine