MEDICINE 2 FOR CN Updated

MEDICINE II FOR CN/EN
KAMPALA UNIVERSITY
SCHOOL OF NURSING AND HEALTH SCIENCES
MEDICAL NURSING II
FOR EN/CN.
"YEAR2/SEM2"
Compiled by;
KIGOZI IBRAHIM TRT Mgt
EN/DNE/Hyp.
0754752081
ibrahimkigozi0240@gmail.com
Inspired by;
Mr. Ssendugga Patrick.
BScN/RN/EN
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Dedication:
I dedicate this literature to Mr. Ssendugga Patrick, a Medical and Pharmacology tutor,
Kampala University School of Nursing who natured me with medical knowledge as a DNE
Student 2022. Through his efforts as my mentor, I possessed the passion of Medicine and
aspiring not to let his efforts perish unnoticed.
Copyright© (2022FEB) By (KIGOZI IBRAHIM)
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CONDITIONS AFFECTING THE DIGESTIVE

SYSTEM.
STOMATITIS.
Stomatitis is a condition characterized by acute inflammation of the mucus membranes of the lips and
mouth with/with out oral ulcerations. When inflammation of the gums and the mouth generally presents
itself, sometimes the term gingivostomatitis is used.
FORMS OF STOMATITIS.
There are several causes of Stomatitis some of which include the following;
 Aphthous stomatitis (canker sores); is the recurrent appearance of mouth ulcers in otherwise
healthy individuals due to a T Cell mediated immune response.
 Angular stomatitis or angular cheilitis; In children a frequent cause is repeated lip-licking, and in
adults it may be a sign of underlying iron deficiency anemia, or vitamin B deficiencies.
 Denture related stomatitis; It appears as reddened but painless mucosa beneath the denture. 90%
of cases are associated with Candida species, and it is the most common form of oral candidiasis.
 Allergic contact stomatitis/ Allergic gingivostomatitis or Allergic contact gingivostomatitis; is a
type IV (delayed) hypersensitivity reaction that occurs in susceptible atopic individuals when
allergens penetrate the skin or mucosa.
 Migratory stomatitis/geographic stomatitis; is an atypical presentation of a condition which
normally presents on the tongue called geographic tongue.
 Herpetic gingivostomatitis; This is inflammation of the mouth caused by herpes simplex virus.
 Irradiation and chemotherapy; Stomatitis may also be caused by chemotherapy, or radiation
therapy of the oropharyngeal area.
 Stomatitis Nicotina/smoker's palatal keratosis; this condition may occur in smokers, especially
pipe smokers. The palate appears dry and cracked, and white from keratosis.
 Chronic ulcerative stomatitis; is characterized by erosions and ulcerations which relapse and remit.
Lesions are located on the buccal mucosa.
 Uremic stomatitis; is a rare form of stomatitis that occurs with kidney failure.
SIGNS AND SYMPTOMS.

 Difficulty in eating or drinking.
 Dehydration if drinking is a problem.
 Irritability.
 Swollen and drooling gums.
 Fever in case of Herpes simplex virus type 1.
 Ulcer in case the blister bursts.
TYPES OF STOMATITIS.
 Canker sore: also known as an aphthous ulcer, is a single pale or yellow ulcer with a red outer ring
or a cluster of such ulcers in the mouth, usually on the cheeks, tongue, or inside the lip.
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 Cold sores: Also called fever blisters, cold sores are fluid-filled sores that occur on or around the
lips. They rarely form on the gums or the roof of the mouth. Cold sores later crust over with a scab
and are usually associated with tingling, tenderness, or burning before the actual sores appear.
CAUSES OF STOMATITIS.
 Infections like herpes simplex virus, bacteria.
 Nutritional deficiencies like Vitamin B1,2,3,6,9 and 12
 Allergic reactions to certain chemicals.
 Radiotherapy and chemotherapy.
 Dentures or braces.
 Chewing tobacco.
 Burning mouth from hot foods.
 Stress.
 Inflammatory bowel diseases.
 Dry tissues from breathing through the mouth due to clogged nasal passages.
 Candida albicans infection.
 Small injuries due to dental work, accidental cheek bite, or other injuries.
 Sharp tooth surfaces.
 Celiac disease.
 Autoimmune diseases that attack cells in the mouth
 HIV/AIDS
 Weakened immune system ①
 Lack of sleep.
 Certain foods like potatoes, citrus fruits, coffee, chocolate, cheese, and nuts.
TESTS AND DIAGNOSIS.

 CBC to check for Neutrophilia incase of infection.
 Culture and Sensitivity to isolate the causative organism.
 A swab in case blisters burst and crast.
PHARMACOLOGICAL CARE.
 Analgesics like Ibuprofen 400mg tds, Diclofenac, Pyroxicam can be used to relieve pain.
 Antibiotics like Ampicillin 50mg/kg, Phenoxymethyl penicillin, Metronidazole can be used in case
of bacterial infection.
 Antivirals like 5% Acyclovir ointment, Valacyclovir can be used in case of viral infection of
Herpes simplex type 1.
 Apply a topical anesthetic such as lidocaine or xylocaine to the ulcer.
 Topical corticosteroid preparation such as triamcinolone dental paste (Kenalog in Orabase 0.1%),
which protects a sore inside the lip and on the gums.
 Blistex and Campho-Phenique may offer some relief of canker sores and cold sores, especially if
applied when the sore first appears.
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NONPHARMACOLOGICAL CARE.
 Rinse with salt water.
 Practice proper dental care.
 Drink plenty of water.
 Avoid hot beverages and foods as well as salty, spicy, and citrus-based foods.
 Gargle with cool water or suck on ice pops if you have a mouth burn.
PREVENTION.
 Refraining from kissing.
 Avoid sharing eating utensils with someone with an open cold sore.
 Avoid vigorous brushing of teeth.
 Avoid hot foods.
 Consume foods reach in vitamins like Vitamin B1,2,3,6,9,12.
COMPLICATIONS.
 Meningoencephalitis.
 Recurrent skin and mouth infections.
 Dissemination of the infection.
 Teeth loss.
GASTRITIS.
Gastritis is a condition characterised by the acute or chronic Inflammation of the lining of the stomach.
Weaknesses in the mucus lining barrier that protects your stomach wall allows your digestive juices to
damage and inflame your stomach lining causing wounds. Gastritis may occur suddenly called Acute
gastritis, or it can occur slowly over time called Chronic gastritis. In some cases, Gastritis can lead to
ulcers/wounds and an increased risk of Stomach cancer. For most people, however, Gastritis isn't serious
and improves quickly with treatment.
FORMS/CATEGORIES OF GASTRITIS.
 Erosive gastritis, for which the common causes are stress, alcohol,some drugs, such as aspirin and
other nonsteroidal anti-inflammatory drugs (NSAIDs), and Crohn's disease.
 Non-erosive gastritis, for which the most common cause is a Helicobacter pylori infection.
CAUSES OF GASTRITIS.
 Bacterial infection. The infection with Helicobacter pylori is among the most common GI human
infections.
 Regular use of pain relievers. such as aspirin, ibuprofen and naproxen. — can cause both acute
Gastritis and chronic Gastritis.
 Older age. Older adults have an increased risk of Gastritis because the stomach lining tends to thin
with age than in young adults.
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 Excessive alcohol use. Alcohol can irritate your stomach lining, which makes your stomach more
likely to be harmed by digestive juices. Excessive alcohol use is more likely to cause acute Gastritis.
 Stress. Severe stress due to major surgery, injury, Burns or severe infections can cause acute
Gastritis.
 Autoimmune Gastritis, Autoimmune Gastritis is more common in people with other autoimmune
disorders, including Type 1 diabetes or vitamin B-12 deficiency.
 HIV/AIDS; This triggers a weak immune system which allows for the lining of the stomach to be
easily invaded by microorganisms.
 Crohn's disease; which involves Inflammation of the bowels.
 Parasitic infections.
 Radiation therapy.
SIGNS AND SYMPTOMS.

 The Cardinal symptom is Central upper/Epigastric pain which is usually reported by every patient
with gastritis.
 Nausea.
 Vomiting which may be clear, green or yellow, blood-streaked or completely bloody depending on
the severity of the stomach inflammation.
 Belching but does not usually relieve stomach pain if present.
 Bloating which may feel like a sense of fullness.
 Early satiety.
 Loss of appetite or anorexia.
 Unexplained weight loss due to fear of pain after eating.

Blood tests:
 Complete blood count to check for infection.
 Serum for Helicobacter pylori antigen.
 Renal and Liver functioning tests.
Other tests include;
 Urinalysis
 Stool analysis for occult blood in the stool.
 Endoscopy, to check for stomach lining inflammation and mucous erosion
 Stomach biopsy, to test for gastritis and cancer.
 Abdominal ultrasound scan.
Aims;
To relieve pain.
To control symptoms.
To prevent further complications.
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NOTE; The management of Gastritis depends on the underlying cause of the condition for example to stop
use of NSAIDS in case they're the causative agents.
 Analgesics like Paracetamol 10 to 15mg/kg is used since its not linked to irritation of the stomach.
 Antibiotics in case of H. Pylori infection including Metronidazole 400mg tds for 10days,
Amoxicillin 500mg tds, Clarithromycin, Ceftriaxone 50mg/kg can be used to eradicate the infection.
 Proton pump inhibitors including Omeprazole 20mg od for 10days, Lansoprazole 20mg od,
Esomeprazole to reduce HCL production.
 Antiemetics like Metoclopramide 10 to 15mg tds can be used to control vomiting and nausea.
 Mucosal protectants/ Cytoprotectives like Misoprostol 200mcg bd or tds till symptoms clear, to
increase mucus production hence preventing contact of the lining with HCL. Bismuth subsalicylate
is also useful in case of NSAIDS irritation.
 Antihistamines like Ranitidine 150mg bd for 10 days or Famotidine, Cimetidine can be used.
SPECIFIC NURSING INTERVENTIONS.

 If the patient is vomiting, give antiemetics.
 Administer I.V. fluids as ordered to maintain fluid and electrolyte imbalance.
 When the patient can tolerate oral feedings, provide a balanced diet that takes into account his food
preference.
 Offer smaller, more frequent servings to reduce the amount of irritating gastric secretions.
 Help patient identify specific foods that cause gastric upset and eliminate them from his diet.
 Administer antacids and other prescribed medications as ordered.
 If pain or nausea interferes with the patient’s appetite, administer pain medications or antiemetics
about 1 hour before meals.
 Monitor the patient’s fluid intake and output and electrolyte levels.
 Assess the patient for presence of bowel sounds.
 Monitor the patient’s response to antacids and other prescribed medications.
 Monitor the patient’s compliance to treatment and elimination of risk factors in his lifestyle.
 Teach the patient about the disorder.
 Urge the patient to seek immediate attention for recurring signs and symptoms, such as hematemesis,
nausea, or vomiting
PREVENTION.
 Avoid stress.
 Cease alcohol intake.
 Stop or reduce cigarette smoking.
 Avoid prolonged use of NSAIDS like Ibuprofen, Naproxen, Pyroxicam, Aspirin, Celecoxib and
more.
 Avoid fatty foods.
 Avoid acidic foods like oranges, lemon etc.
COMPLICATIONS.
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 Gastrointestinal perforation.
 Rarely, stomach cancer.
 Weight loss.
PEPTIC ULCER DISEASE (PUD).

Peptic Ulcer Disease is a condition characterised by the breakage of the mucus lining or membrane of the
gastrointestinal tract making it get into contact with hydrochloric acid. Its usually caused by Helicobacter
Pylori, Its helical shape from which the genus name "helicobacter" derives, is thought to have evolved in
order to penetrate the mucoid lining of the stomach and thereby establish infection. The H. Pylori is a
normal flora within the gastrointestinal tract.
FORMS/TYPES OF PUD.
 Oesophageal ulcers; these happen within the oesophagus running from the mouth to cardiac
sphincter.
 Gastric ulcers; these happen within the stomach.
 Duodenal ulcers; these happen within the duodenum, the first portion of the small intestine from
the stomach.
 Stress ulcers; these happen anywhere within the gastrointestinal tract due to conditions like surgery,
burns, chronic illness.
CAUSES OF PUD.
The exact cause of PUD is Helicobacter Pylori infection. The rest are risk factors which include the
following;
 Regular use of pain relievers. such as aspirin, ibuprofen and naproxen.
 Older age. Older adults have an increased risk of Gastritis because the stomach lining tends to thin
with age than in young adults.
 Excessive alcohol use. Alcohol can irritate your stomach lining, which makes your stomach more
likely to be harmed by digestive juices. Excessive alcohol use is more likely to cause acute Gastritis.
 Stress. Severe stress due to major surgery, injury, Burns or severe infections can cause acute
Gastritis.
 HIV/AIDS; This triggers a weak immune system which allows for the lining of the stomach to be
easily invaded by microorganisms.
 Radiation therapy.
 Prolonged cigarette smoking.
 Irregular meals.
SIGNS AND SYMPTOMS.

The most common symptom of PUD is PAIN.
 Pain usually after having a meal in case of gastric ulcers.
 Pain usually relieved by food in case of duodenal ulcers.
 Night flares called Hourglass contracture common in duodenal ulcers.
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 Nausea and vomiting.

 Constipation.
 Headaches.
 Loss of appetite.
 Unexplained weight loss due to fear of pain after a meal.
 Hemetemesis in case of severe ulcers.
 Black tarry stool in case of upper GI bleeding.

Aims;
To relieve pain.
To control signs and symptoms.
Physical examination of the abdomen can help to locate sites of pain which may help to isolate the type of
ulcer.
Blood tests for;
 Serum for Helicobacter pylori antigen. The current UCG 2020 Guidelines phased out this test and
resorted to the Stool analysis for H. Pylori bacterium.
 Complete blood count to check for infection.
 Blood culture to isolate H. Pylori bacterium.
 Stool for occult blood.
 Upper endoscopy to check for GI erosion.
 Abdominal ultra sound scan.
 Abdominal Xrays.
 A tissue biopsy to rule out cancer and other Infections.
 Triple therapy; this acts as the "First line regimen" and comprises of Metronidazole 400mg tds +
Amoxicillin 500mg tds + Omeprazole 20mg od all together for 7 to 14 days, with Paracetamol 1g
tds for 1 week.
 Quadruple therapy; This is the "Second line regimen" and involves the combination of
Metronidazole + Amoxicillin + Clarithromycin + Omeprazole all together for 14 days. Incase of
resistance with this regimen, Clarithromycin can be replaced with any Tetracycline group like
Doxycycline, Tetracycline.
 Antiemetics like Metoclopramide 10 to 15mg tds can be used to control vomiting and nausea.
 Mucosal protectants/ Cytoprotectives like Misoprostol 200mcg bd or tds till symptoms clear,
Bismuth subsalicylate is also useful in case of NSAIDS irritation. Misoprostol should be used with
caution in women due to risk of abortion.
 Antihistamines like Ranitidine 150mg bd for 10 days or Famotidine, Cimetidine can be used.
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 Antacids; these include Magnesium trisilicate to reduce acid levels within the stomach.

 Support the patient emotionally and offer reassurance.
 Administer prescribed medications.
 Provide six small meals a day or small hourly meals as ordered.
 Schedule care so that the patient gets plenty of rest.
 Monitor the effectiveness of administered medications, and also watch for adverse reactions.
 Assess the patient’s nutritional status and the effectiveness of measures used to maintain it. Weigh
him regularly.
 Teach the patient about peptic ulcer disease, and help him to recognize its signs and symptoms.
 Review the proper use of prescribed medications, dicussing the desired actions and possible adverse
effect of each drug.
 Instruct the patient to take antacids 1 hour after meals.
 Warn the patient to avoid aspirin containing drugs because they irritate gastric mucosa.
 Encourage the patient to make appropriate lifestyle changes.
PREVENTION OF PUD.
 Adequate hand washing to avoid food contamination.
 Food should be cooked thoroughly.
 Avoid excessive use of NSAIDS like Ibuprofen, naproxen and more.
 Cease alcohol intake.
 Cease cigarette smoking.
 Maintain regular meals.
COMPLICATIONS OF PUD.
 Gastrointestinal perforation.
 Gastric or duodenal cancer.
 Malabsorption syndrome.
 Weight loss.
 Poor drug absorption.
JAUNDICE.
Jaundice or Icterus, is a yellowish pigmentation of the skin and whites of the eyes due to high bilirubin
levels in blood.
Jaundice in adults is typically a sign indicating the presence of underlying diseases involving abnormal
heme metabolism, liver dysfunction, or biliary tract obstruction. The prevalence of jaundice in adults is rare,
while jaundice in babies is common, with an estimated 80% affected during their first week of life. Infant
jaundice usually occurs because a baby's liver isn't mature enough to get rid of bilirubin in the bloodstream.
In some cases, an underlying disease may cause jaundice.
NOTE: Jaundice is present when blood levels of bilirubin exceed 3 mg/dL.
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CAUSES OF JAUNDICE.
1. Prehepatic causes (hemolytic);
Prehepatic jaundice is most commonly caused by a pathological increased rate of red blood cell hemolysis.
The increased breakdown of erythrocytes leading to increased unconjugated serum bilirubin hence causing
increased deposition of unconjugated bilirubin into mucosal tissue. These diseases may cause jaundice due
to increased erythrocyte hemolysis:
 Sickle cell anemia.
 Spherocytosis.
 Thalassemia.
 Pyruvate kinase deficiency.
 Glucose-6-phosphate dehydrogenase deficiency.
 Microangiopathic hemolytic anemia.
 Hemolytic uremic syndrome.
 Severe malaria.
2. Hepatic causes (hepatocellular);

Hepatic jaundice is caused by abnormal liver metabolism of bilirubin. The major causes of hepatic jaundice
are significant damage to hepatocytes due to infectious diseases, drug induced conditions, autoimmune
etiology, or less commonly, due to inheritable genetic diseases. The following are the hepatic causes to
jaundice:
 Acute hepatitis.
 Chronic hepatitis.
 Hepatotoxicity.
 Cirrhosis.
 Drug-induced hepatitis.
 Alcoholic liver disease.
 Gilbert's syndrome; its found in about 5% of the population.
 Crigler-Najjar syndrome type I and type II.
 Leptospirosis.
3. Post hepatic causes (obstructive);

Posthepatic jaundice (obstructive jaundice), is caused by a blockage of bile ducts that transport bile
containing conjugated bilirubin out of the liver for excretion. Available causes include;
 Choledocholithiasis; as the most common cause.
 Pancreatic cancer of the pancreatic head.
 Biliary tract strictures.
 Biliary atresia.
 Primary biliary cholangitis.
 Cholestasis of pregnancy.
 Acute Pancreatitis.
 Chronic Pancreatitis.
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 Pancreatic pseudocysts.
RISK FACTORS TO JAUNDICE.

 Premature birth. A baby born before 38 weeks may not be able to process bilirubin as quickly as
full-term babies do. Also, he or she may feed less and have fewer bowel movements, resulting in
less bilirubin eliminated through stool.
 Significant bruising during birth. If your newborn gets bruises from the delivery, he or she may
have a higher level of bilirubin from the breakdown of more red blood cells.
 Blood type. If the mother's blood type is different from her baby's, the baby may have received
antibodies through the placenta that cause his or her blood cells to break down more quickly.
 Breast-feeding. Dehydration or a low calorie intake may contribute to the onset of jaundice.
SIGNS AND SYMPTOMS OF JAUNDICE.

 Yellowish discoloration of the sclera and skin indicating a serum bilirubin of at least 3 mg/dl.
 Dark urine (bilirubinuria).
 Pale urine (acholia).
 Fatty stool (steatorrhea).
 Severe itchiness.

The tests are centered at measuring the level of bilirubin in circulation to determine the treatment.
 A physical exam is key.
 A blood sample to check for: Total serum bilirubin, Conjugated and unconjugated bilirubin.
 Urinalysis for color, urobilinogen.
 A skin test with a device called a transcutaneous bilirubinometer.
 Alanine transferase and aspartate transferase levels.
 Abdominal ultrasound scan, CT Scan.
 Phototherapy; Your baby may be placed under special lighting that emits light in the blue-green
spectrum. The light changes the shape and structure of bilirubin molecules in such a way that they
can be excreted in the urine and stool.
 Intravenous immunoglobulin (IVIg). Intravenous transfusion of an immunoglobulin, a blood
protein that can reduce levels of antibodies may decrease jaundice and lessen the need for an
exchange blood transfusion.
 Exchange transfusion. Rarely, a baby may need an exchange transfusion of blood. This involves
repeatedly withdrawing small amounts of blood, diluting the bilirubin and maternal antibodies, and
then transferring blood back into the baby.
 Incase the above fail, surgery can be opted to correct the bilirubin channels.
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Aims;
To restore normal liver function.
To eradicate the cause.
 Assess the color of skin, sclera of eye and mucous membrane of mouth and nose every 8 hours.
 Check for any sign of complication and notify the physician.
 Check neurological status 8 hourly to identify complication of bilirubin encephalopathy.
 Check vital signs every 4 hourly.
 Monitor intake output and check urine and stool color.
 Administer medication as ordered.
 Control nausea and vomiting and administer anti-emetic drug as ordered.
 Monitor direct and indirect bilirubin to evaluate treatment efficacy.
 Provide healthy diet.
 Give mouth care to increase appetite and prevent vomiting. Provide low fat diet.
 Encourage patient to take plenty of fluids(at least 6-8 glass daily)
 Check weight daily to evaluate weight loss or gain.
 Administer IV fluid (if diarrhea is present)
 Ensure proper rest and keep everything at reach for the patient.
 Keep skin clean and dry to prevent itching.
 Provide health education to patient and family members on how to prevent jaundice.
 Arrange vaccination program and administer vaccine to patient as ordered.
 Provide psychological support to patient and encourage the patient express his/her feelings.
COMPLICATIONS OF JAUNDICE.
 Kernicterus.
 Kidney failure.
 Constipation.
 Anemia.
 Edema.
HEPATITIS (Hep).
Hepatitis is a condition characterized by the acute inflammation of the liver tissue. Hepatitis is acute if it
resolves within 6 months, and chronic if it lasts longer than 6 months. Acute hepatitis can resolve on its
own or progress to chronic hepatitis, or rarely result in acute liver failure. Chronic hepatitis may progress to
scarring of the liver (cirrhosis), liver failure, and liver cancer.
CAUSES OF HEPATITIS.
Viral hepatitis;
This is caused by 5 species that are the most common;
 Hepatitis A transmitted via fecal oral route.
 Hepatitis B.
 Hepatitis C. These 3 are transmitted via bodily fluids like blood, urine.
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 Hepatitis D.
 Hepatitis E transmitted via fecal oral route.
Genetic factors;
 Alpha-1-antitrypsin deficiency.
 Hemochromatosis.
 Wilson's disease
Toxic and drug-induced hepatitis;
 Analgesic paracetamol.
 Antibiotics such as isoniazid, nitrofurantoin, amoxicillin-clavulanate, erythromycin, and
trimethoprim-sulfamethoxazole.
 Anticonvulsants such as valproate and phenytoin.
 Cholesterol-lowering statins like atovastatin, simvastatin.
 Steroids such as oral contraceptives and anabolic steroids.
 Highly active anti-retroviral therapy used in the treatment of HIV/AIDS.
Alcoholic hepatitis;
 This arises from prolonged alcohol consumption.
Bacterial infection causing;
 Pyogenic liver abscesses.
 Acute hepatitis.
 Granulomatous or chronic liver disease.
Parasitic hepatitis;
Among the parasites, the following are responsible for liver inflammation;
 Trypanosoma cruzi.
 Leishmania species.
 Malaria causing Plasmodium species.
Fulminant Hepatitis;
Is a rare but severe complication of hepatitis, which may require liver transplantation.
SIGNS AND SYMPTOMS OF HEPATITIS.

Hepatitis usually has self limiting symptoms and keep on advancing as the disease progresses.
Acute hepatitis; This follows 3 distinctive phases namely;
The initial prodromal phase: involves non specific symptoms including fatigue.
 Nausea.
 Vomiting.
 Poor appetite.
 Joint pain.
 Headaches.
 Fever, when present, is most common in cases of hepatitis A and E. Late in this phase.
 Choluria (dark urine) and clay-colored stools.
Yellowing of the skin and sclera:
 This usually sets in 1-2 weeks after the first phase and lasts for 4 weeks.
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 The non specific symptoms typically fade away by this time.

 Hepatomegally sets in.
 Right upper abdominal pain is common.
 Splenomegally in 10–20%.
 Mild unintentional weight loss.
The recovery phase:
This involves the gradual resolution of the typical symptoms of hepatitis, but;
 Persistent elevations in liver lab values.
 Persistent hepatomegally.
 All cases of hepatitis A and E are expected to fully resolve after 1–2 months.
 Most hepatitis B patients will recover in 3–4 months.
 Few cases of hepatitis C will resolve completely.
Chronic hepatitis;
 This is detected only by liver laboratory studies for screening purposes or to evaluate non specific
symptoms.
 Fatigue.
 Nausea and vomiting
 Poor appetite and joint pain.
 Jaundice can occur as well.
 Acne.
 Hirsutism or abnormal hair growth.
 Amenorrhea in women.
 Weight loss.
 Coagulopathy.
 Ascites (abdominal fluid collection).
 Peripheral edema (leg swelling).
 Hepatic encephalopathy.
 Esophageal varices.
 Hepatorenal syndrome and liver cancer.

 Physical examination.
 Blood samples for Renal function tests (RFT) and Liver function tests (LFT).
 Blood samples for complete blood count to check for infection.
 Immunoglobulin M (IgM) antibodies to hepatitis A virus in the acute phase.
 Radioimmunoassays to detect hepatitis B surface antigen (HBsAg).
 Urinalysis.
 Ascitic fluid samples for culture.
 Magnetic resonance imaging (MRI). Abdominal ultrasound scan and CT Scan.
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The treatment of hepatitis varies according to the type, whether it is acute or chronic, and the severity of the
disease.
Aims;
To restore normal liver function.
 Vitamin K injected subcutaneously (S.C.) if prothrombin time is prolonged.
 I.V. fluid and electrolyte replacements as indicated.
 Antiemetic for nausea and vomiting.
Hepatitis A;
 Usually does not progress to a chronic state, and rarely requires hospitalization. Treatment is
supportive and includes such measures as providing intravenous (IV) hydration and maintaining
adequate nutrition.
Hepatitis B;
 Acute phase requires Tenofovir (TDF) or Entecavir.
 Chronic phase; 7 kinds of drugs we're approved for use including; Pegylated interferon (PEG IFN)
is dosed just once a week as a subcutaneous injection. Lamivudine. Tenofovir. Entecavir.
Telbivudine. Adefovir depivoxil.
Hepatitis C;
The required treatment is as follows;
 NS3/4A protease inhibitors, including Telaprevir, Bboceprevir, Simeprevir.
 NS5A inhibitors, including Ledipasvir, Daclatasvir.
 NS5B polymerase inhibitors, including Sofosbuvir, Dasabuvir.
Hepatitis D;
 This is difficult to treat, and effective treatments are lacking. Interferon alpha has proven effective at
inhibiting viral activity but only on a temporary basis.
Alcoholic and Autoimmune hepatitis;
These require high doses of corticosteroids to slow disease progress.

 Monitor hydration through intake and output.
 Monitor prothrombin time and for signs of bleeding.
 Encourage the patient to eat meals in a sitting position to reduce pressure on the liver.
 Encourage pleasing meals in an environment with minimal noxious stimuli (odors, noise, and
interruptions).
 Teach self administration of antiemetics as prescribed.
 Encourage rest during symptomatic phase, according to level of fatigue.
 Encourage diversional activities when recovery and convalescence are prolonged.
 Encourage gradual resumption of activities and mild exercise during convalescent period.
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 Stress importance of proper public and home sanitation and proper preparation and dispensation of
foods.
 Encourage specific protection for close contacts.
 Explain precautions about transmission and prevention of transmission to others to the patient and
family.
 Warn the patient to avoid trauma that may cause bruising.
 Stress the need to follow precautions with blood and secretions until the patient is deemed free of
HBsAg.
 Emphasize that most hepatitis is self-limiting, but follow up is needed for liver function tests.
COMPLICATIONS.
 Liver cancer.
 Liver failure.
 Liver cirrhosis.
 Kidney failure.
LIVER CIRRHOSIS (LC).

Liver cirrhosis or End stage liver disease is a condition characterised by an impairment in liver function
caused by scar tissue called fibrosis resulting from previous liver diseases.
The liver carries out several necessary functions, including detoxifying harmful substances in your body,
cleaning your blood and making vital nutrients. Cirrhosis occurs in response to damage to your liver. The
liver damage done by cirrhosis can't be undone. But if liver cirrhosis is diagnosed early and the cause is
treated, further damage can be limited. As cirrhosis progresses, more and more scar tissue forms, making it
difficult for the liver to function (decompensated cirrhosis). Advanced cirrhosis is life-threatening.
CAUSES OF LIVER CIRRHOSIS.

Some of the causes of cirrhosis are inherited or thought to be inherited:
 Hemochromatosis (Iron buildup in the body).
 Cystic fibrosis.
 Wilson's disease (Copper accumulated in the liver).
 Biliary atresia.
 Galactosemia or glycogen storage disease.
 Alagille syndrome.
 Autoimmune hepatitis.
Others occur later in life:
 Chronic alcohol abuse.
 Hepatitis C.
 Hepatitis B.
 Nonalcoholic fatty liver disease.
 Primary biliary cirrhosis.
 Primary sclerosing cholangitis (Hardening and scarring of the bile ducts).
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 Schistosomiasis infection.
SIGNS AND SYMPTOMS OF LC.

Cirrhosis often has no signs or symptoms until liver damage is extensive. When signs and symptoms do
occur, they may include:
 Fatigue.
 Bleeding easily.
 Bruising easily.
 Itchy skin.
 Yellow discoloration in the skin and eyes (jaundice).
 Severe ascites.
 Nausea.
 Swelling in your legs or edema.
 Weight loss.
 Confusion, drowsiness and slurred speech indicating hepatic encephalopathy.
 Spider like blood vessels on your skin.

 Liver biopsy; the gold standard test for liver cirrhosis which maybe percutaneous or transjugular
fine needle approach.
 Endoscopic ultrasound guided liver biopsy (EUS), using the percutaneous or transjugular route is
done.
 Serum for C- Reactive Protein (CRP) and Procalcitonin
 Aminotransferases AST and ALT are moderately elevated.
 Alkaline phosphatase; slightly elevated but less than 2–3 times the upper limit of normal.
 Bilirubin levels are normal when compensated, but may elevate as cirrhosis progresses.
 serum for Albumin levels which are usually high.
 Prothrombin time increases, since the liver synthesizes clotting factors.
 Leukopenia and Neutropenia are due to splenomegaly with splenic margination.
 Blood for electrolytes especially sodium levels.
 Clotting factors test.
 FibroTest is a biomarker for fibrosis that may be used instead of a biopsy.
 MRI, CT Scan and abdominal ultrasound scan.
NOTE; The above tests are "typical" in liver cirrhosis testing.
Aims;
To slow progression of scar tissue.
To alleviate signs and symptoms.
To eradicate the cause of the disease.
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 Octreotide. If required, octreotide may be prescribed for esophageal varices.
 Diuretics. Diuretics may be given for edema, however, they require careful monitoring because
fluid and electrolyte imbalance may precipitate hepatic encephalopathy.
 Lactulose. Encephalopathy is treated with lactulose.
 Antibiotics. Antibiotics are used to decrease intestinal bacteria and reduce ammonia production, one
of the causes of encephalopathy.
 Transjugular intrahepatic portosystemic shunt (TIPS) procedure. The TIPS procedure is used for the
treatment of varices by upper endoscopy with banding to relieve portal hypertension.
Treatment for alcohol dependency. People with cirrhosis caused by alcohol abuse should try to stop
drinking.
 Weight loss. People with cirrhosis caused by Nonalcoholic fatty liver disease may become healthier
if they lose weight and control their blood sugar levels.
 Medications to control Hepatitis. Medications may control damage to liver cells caused by Hepatitis
B or C.
 Portal hypertension. Blood pressure medications may control increased pressure in the veins that
supply the liver.
 Infections. You may receive antibiotics or other treatments for infections.

Position bed for maximal respiratory efﬁciency; provide oxygen if needed.
Initiate efforts to prevent respiratory, circulatory, and vascular disturbances.
Encourage patient to increase activity gradually and plan rest with activity and mild exercise.
Improving Nutritional Status;
 Provide a nutritious, high-protein diet supplemented by B-complex vitamins and others, including A,
C, and K.
 Encourage patient to eat: Provide small, frequent meals, consider patient preferences, and provide
protein supplements, if indicated.
 Provide nutrients by feeding tube or total PN if needed.
 Provide patients who have fatty stools (steatorrhea) with water-soluble forms of fat-soluble vitamins
A, D, and E, and give folic acid and iron to prevent anemia.
 Provide a low-protein diet temporarily if patient shows signs of impending or advancing coma;
restrict sodium if needed.
Providing Skin Care;
 Change patient’s position frequently.

 Avoid using irritating soaps and adhesive tape.
 Provide lotion to soothe irritated skin; take measures to prevent patient from scratching the skin.
Reducing Risk of Injury;
 Use padded side rails if patient becomes agitated or restless.
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 Orient to time, place, and procedures to minimize agitation.

 Instruct patient to ask for assistance to get out of bed.
 Carefully evaluate any injury because of the possibility of internal bleeding.
 Provide safety measures to prevent injury or cuts (electric razor, soft toothbrush).
 Apply pressure to venipuncture sites to minimize bleeding.
Monitoring and Managing Complications;
 Monitor for bleeding and hemorrhage.
 Monitor the patient’s mental status closely and report changes so that treatment of encephalopathy
can be initiated promptly.
 Carefully monitor serum electrolyte levels are and correct if abnormal.
 Administer oxygen if oxygen desaturation occurs; monitor for fever or abdominal pain, which may
signal the onset of bacterial peritonitis or other infection.
 Assess cardiovascular and respiratory status; administer diuretics, implement ﬂuid restrictions, and
enhance patient positioning, if needed.
 Monitor intake and output, daily weight changes, changes in abdominal girth, and edema formation.
 Monitor for nocturia and, later, for oliguria, because these states indicate increasing severity of liver
dysfunction.
COMPLICATIONS.
 Portal hypertension.
 Hemorrhage.
 Edema.
 Kidney failure.
 Heart disease.
CHOLECYSTITIS.
Cholecystitis is the acute inflammation of the gall bladder. Your gallbladder is a small, pear-shaped organ
on the right side of your abdomen, beneath your liver. The gallbladder holds a digestive Fluid that's released
into your small intestine (bile). In most cases, Gallstones blocking the tube leading out of your gallbladder
cause Cholecystitis. This results in a bile buildup that can cause inflammation. Other causes of Cholecystitis
include bile duct problems and Tumors. If left untreated, Cholecystitis can lead to serious, sometimes life-
threatening complications, such as a gallbladder rupture.
CAUSES OF CHOLECYSTITIS.
 Acute calculous cholecystitis; gallstones blocking the flow of bile account for 90% of cases of
cholecystitis.
 Acalculous cholecystitis; It accounts for 5–10% of all cases of cholecystitis and is associated with
high morbidity and mortality rates.
 Chronic cholecystitis due to long standing acute cholecystitis.
 Xanthogranulomatous cholecystitis.
 Tumors which block flow of bile.
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 Kinking of bile duct.
SIGNS AND SYMPTOMS.

 Pain typically sets in after a heavy meal due to compression of the gallbladder.
 Severe pain at upper right abdomen.
 Pain that radiates from the right shoulder or back.
 Leucocytosis.
 Pain upon inspiration during palpation (Murphy's Sign).
 Abdominal tenderness and rigidity.
 Indigestion.
 Belching.
 Flatulence.
 Tenderness over your abdomen when it's touched.
 Nausea.
 Sepsis or bactereamia.
 Vomiting.
 Fever.
 Tachycardia.
 Signs of dehydration.

 Cholecystography.
 Percutaneous transhepatic cholangiography.
 Endoscopic retrograde cholangiopancreatography (ERCP): Visualizes biliary tree by cannulation of
the common bile duct through the duodenum.
 Abdominal xray. Radiopaque or calcified gallstones present in 10% to 15% of cases.
 Blood for CBC to check for infection.
 Abdominal ultrasound scan to view bladder size and rule out gallstones.
 Abdominal MRI, CT Scan can be done.
 A hepatobiliary iminodiacetic acid (HIDA) scan tracks the production and flow of bile from your
liver to your small intestine and shows blockage.
Aims;
Relieve pain and promote rest.
Maintain fluid and electrolyte balance.
Prevent complications.
Provide information about disease process, prognosis, and treatment needs.
 Fasting which maybe done to take pressure off your inflamed gallbladder.
 IV Fluids to correct dehydration due to fasting.
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 Antibiotics to fight infection like Metronidazole 400mg tds or Levofloxacin 500mg od are
commonly used. Others include; Phenoxymethyl penicillin V 400mg qid or Ceftriaxone 50mg/kg od.
 Analgesics like Ibuprofen 400mg tds to relieve pain.
 Promethazine to control nausea and vomiting.
 Anti chili ethics to reduce muscle spasms and control pain.
 Antiinflammatory agents like hydrocortisone 100-200mg od or bd to reduce the rate of inflammation.

 Pain assessment. Observe and document location, severity (0-10 scale), and character of pain.
 Activity. Promote bed rest, allowing the patient to assume a position of comfort.
 Diversion. Encourage use of relaxation techniques, and provide diversional activities.
 Communication. Make time to listen and to maintain frequent contact with the patient.
 Calories. Calculate caloric intake to identify nutritional deficiencies or needs.
 Food planning. Consult the patient about likes and dislikes, foods that cause distress, and preferred
meal schedules.
 Promote appetite. Provide a pleasant atmosphere at mealtime and remove noxious stimuli.
 Laboratory studies. Monitor laboratory studies: BUN, pre-albumin, albumin, total protein,
transferrin levels.
COMPLICATIONS.
 Acute cholecystitis.
 Acute pancreatitis.
 Ascending cholangitis.
 Gangrenous gallbladder. (most common)
 Cholecystocholedochal fistula.
 Gallstone ileus.
CONDITIONS AFFECTING THE URINARY

SYSTEM.
URETHRITIS.
Urethritis is a renal condition characterised by the inflammation of the urethra. The urethra is the tube that
connects the urinary bladder to the external environment.
CAUSES OF URETHRITIS.
 Neisseria gonorrhea also called Gonococcal urethritis.
 Chlamydia trachomatis also called Non Gonococcal urethritis/Non specific urethritis.
Other causes include:
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 Mycoplasma genitalium: second most common cause accounting for 15-20% of non-gonococcal
urethritis
 Trichomonas vaginalis: accounts for 2-13% of cases.
 Adenoviridae.
 Uropathogenic Escherichia coli (UPEC).
 Herpes simplex virus.
 Cytomegalovirus.
 Reactive arthritis: urethritis is part of the triad of reactive arthritis, which includes arthritis, urethritis,
and conjunctivitis.
 Ureaplasma urealyticum.
 Methicillin-resistant Staphylococcus aureus.
 Group B streptococcus.
 Irritation from agents like soap, right pants.
SIGNS AND SYMPTOMS OF URETHRITIS.

 Frequency of micturation.
 Urgency of micturation.
 Burning during micturation.
 Dysuria.
 Urethral discharge.
 Dyspereunia.
 Hematuria especially in men.
 Painfull ejaculation.
 Painful erections and discomfort during sexual intercourse.

 Urinalysis.
 Blood for CBC to check for infection.
 Urine culture.
 Pus swab for microscopy.
 Abdominal ultrasound scan.
Aims;
To relieve signs and symptoms.
 Antibiotics taken by mouth such as trimethoprim/sulfamethoxazole 960mg bd for 1 week,
nitrofurantoin, or fosfomycin are typically first line.
 Cephalosporins like Ceftriaxone 50mg/kg od as prescribed, amoxicillin/clavulanic acid 750mg tds,
or a fluoroquinolone like Ciprofloxacin 500mg bd, Ofloxacin 200mg may also be used.
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 An Intravenous route of the desired antibiotic can be opted for incase of severe Cystitis.
 Analgesia like Ibuprofen 400mg tds can be given.
 Paracetamol 10-15mg/kg for fever.
COMPLICATIONS.
 Penile edema.
 Reactive arthritis incase of Gonococcal urethritis.
 Miscarriages.
 Pyelonephritis.
 Cystitis.
CYSTITIS.
Cystitis is the acute inflammation of the urinary bladder characterised by lower abdominal discomfort.
Most of the time, the inflammation is caused by a bacterial infection, and it's called a UTI. A bladder
infection can be painful and annoying, and it can become a serious health problem if the infection spreads to
your kidneys. Less commonly, Cystitis may occur as a reaction to certain drugs, radiation therapy or
potential irritants, such as feminine hygiene spray, spermicidal jellies or long-term use of a catheter. The
usual treatment for bacterial Cystitis is antibiotics. Treatment for other types of Cystitis depends on the
underlying cause.
CAUSES OF CYSTITIS.
 Bacterial factors; these include E. Coli, Staphylococcus saprophyticus.
 Non infectious factors; Interstitial cystitis also called Painful bladder syndrome.
 Drug-induced Cystitis. chemotherapy drugs cyclophosphamide and ifosfamide, can cause
inflammation of your bladder as the broken-down components of the drugs exit your body.
 Radiation Cystitis. Radiation treatment of the pelvic area can cause inflammatory changes in
bladder tissue.
 Foreign-body Cystitis. Long-term use of a catheter can predispose you to bacterial infections and to
tissue damage, both of which can cause inflammation.
 Chemical Cystitis. feminine hygiene sprays or spermicidal jellies, and may develop an allergic-type
reaction within the bladder, causing inflammation.
 Diabetes mellitus.
 Kidney stones.
 An enlarged prostate.
 Spinal cord injuries.
SIGNS AND SYMPTOMS.

Cystitis signs and symptoms often include:
 A strong, persistent urge to urinate.
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 A burning sensation when urinating.

 Passing frequent, small amounts of urine.
 Blood in the urine (Hematuria).
 Passing cloudy or strong-smelling urine.
 Pelvic discomfort.
 A feeling of pressure in the lower abdomen.
 Low-grade Fever.

 Physical examination of fever, lower abdominal pain and urine issues can help in the diagnosis.
 Urinalysis or Urine culture.
 Abdominal ultrasound, CT Scan, MRI can be done.
PHARMACOLOGICAL MANAGEMENT
 Antibiotics taken by mouth such as trimethoprim/sulfamethoxazole 960mg bd for 1 week,
 An Intravenous route of the desired antibiotic can be opted for incase of severe Cystitis.
COMPLICATIONS.
 Chronic kidney injury.
 Hematuria.
 Anemia.
PYLONEPHRITIS.
Pyelonephritis is an acute upper urinary tract infection that involves inflammation of one or both kidney
pelvis. Generally, Pyelonephritis begins in your urethra or bladder and travels up into your kidneys. A
Kidney infection requires prompt medical attention. If not treated properly, a Kidney infection can
permanently damage your kidneys or the bacteria can spread to your bloodstream and cause a life-
threatening infection. Kidney infection treatment usually includes antibiotics and often requires
hospitalization.
CAUSES OF PYELONEPHRITIS.
 Typically occurs when bacteria enter your urinary tract through the urethra and begin to multiply.
 Septiceamia.
 Rarely, if you have an artificial joint or heart valve that becomes infected.
 Rarely, after kidney surgery.
RISK FACTORS OF PYELONEPHRITIS.

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 Female anatomy. A woman's urethra is much shorter than a man's, so bacteria have less distance to
travel from outside the body to the bladder.
 Obstruction in the urinary tract. such as a kidney stone, structural abnormalities.
 Benign Prostate Hyperplasia can increase your risk of Kidney infection.
 Weakened immune system. such as Diabetes and HIV, increase your risk of Kidney infection.
 Certain medications, such as drugs taken to prevent rejection of transplanted organs, have a similar
effect on reducing immune systems effect.
 Damage to nerves around the bladder. so that you're unaware when it's advancing to a Kidney
infection.
 Prolonged use of a urinary catheter.
 In Vesicoureteral reflux, small amounts of urine flow from your bladder back up into your ureters
and kidneys.
SIGNS AND SYMPTOMS.

 Fever.
 Persistent hypertension and proteinuria maybe the first indicator.
 Loin pain.
 Abdominal pain.
 Frequent urination.
 Strong, persistent urge to urinate.
 Burning sensation or pain when urinating..
 Hematuria and Pyuria.
 Tender prostate gland.
 Occasional weakness.
 History of Cystitis.
 Rigors due to high fevers.
 Anemia.
CLASSIFICATION OF PYELONEPHRITIS.
Pyelonephritis is classified into 3 classes;
1. Acute Pyelonephritis; This is an exudative purulent localized inflammation of the renal pelvis. This
usually consists of pus, neutrophils, fibrin and cell debris. In its early stages, the glomerulus and
vessels are normal, gross pathology reveals radiating bleeding and suppuration through renal pelvis
and cortex.
2. Chronic Pyelonephritis; this is the recurrent kidney infections and leads to scarring of the kidney
parenchyma and impaired function especially due to obstruction. In severe cases, it may cause
perinephric abscess, Pyonephrosis.
3. Xanthogranulomatous; its an unusual form of chronic Pyelonephritis characterised by
granulomatous abscess formation, severe kidney destruction, a clinical picture of renal cell cancer
and other kidney parenchyma diseases. Signs and symptoms often are;
 Fever.
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 Urosepsis.
 Anemia.
 Painful kidney mass.
 Bacterial cultures are usually positive.
 Management is by Nephrectomy (surgical removal of the kidney).

 Physical examination of fever, back pain and urine issues can help in the diagnosis.
 Urinalysis.
 Abdominal ultrasound, CT Scan, MRI can be done.
 Blood sample for RFTs and LFTs.
 CBC to check for neutrophils.
 Blood culture to isolate causative organism.
 Urine culture.
 Blood analysis may indicate hypercalcaemia.
PHARMACOLOGICAL MANAGEMENT.
Usually an OPD protocol is opted for;
 Antibiotics taken by mouth such as trimethoprim/sulfamethoxazole 960mg bd for 1-2 weeks,
 An Intravenous route of the desired antibiotic can be opted for incase of severe Pyelonephritis.
LIFESTYLE CHANGES/ PATIENTS CONSIDERATIONS.

 Drink plenty of Fluids, especially water. Drinking Fluids can help remove bacteria from your body
when you urinate.
 Urinate frequently. Avoid delaying urination when you feel the urge to urinate.
 Empty the bladder after intercourse. Urinating as soon as possible after intercourse helps clear
bacteria from the urethra, reducing your risk of infection.
 Wipe carefully. Wiping from front to back after urinating and after a bowel movement helps prevent
bacteria from spreading to the urethra.
 Avoid using feminine products in the genital area. Using feminine products, such as deodorant
sprays or douches, in your genital area can irritate your urethra.
COMPLICATIONS.
 Chronic kidney injury.
 Septicemia.
 Premature labor and low birth weight babies.
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GLOMERULONEPHRITIS.
Glomerulonephritis or Glomerular disease is a kidney condition characterised by an inflammation of the
filtering system of the kidney and tiny blood vessels within.
Glomeruli remove excess Fluid, electrolytes and waste from your bloodstream and pass them into your
urine. Glomerulonephritis can be Acute with a sudden attack of inflammation or Chronic coming on
gradually.
CAUSES OF GLOMERULONEPHRITIS.
Conditions that can lead to inflammation of the kidneys' glomeruli may include:
Infections;
 Post-streptococcal Glomerulonephritis. Glomerulonephritis may develop a week or two after
recovery from a Strep throat infection or, rarely, a skin infection (Impetigo).
 Bacterial Endocarditis. Bacterial Endocarditis is associated with glomerular disease, but the exact
connection between the two is unclear.
 Viral infections. Viral infections, such as the HIV, Hepatitis B and Hepatitis C.
Immune diseases;
 Lupus erythematosus. Lupus can affect many parts of your body, including your skin, joints, kidneys,
blood cells, heart and lungs.
 Goodpasture's syndrome. Goodpasture's syndrome causes bleeding in your lungs as well as
Glomerulonephritis.
 IgA nephropathy. This primary glomerular disease results from deposits of immunoglobulin A (IgA)
in the glomeruli.
 Vasculitis
 Polyarteritis. This form of Vasculitis affects small blood vessels in many parts of your body like
kidneys and intestines.
 Wegener's granulomatosis. This form of Vasculitis affects small and medium blood vessels in your
lungs, upper airways and kidneys.
 High blood pressure. High blood pressure can damage your kidneys and impair their ability to
function normally.
 Diabetic nephropathy; can affect anyone with Diabetes.
 Focal segmental glomerulosclerosis. Characterized by scattered scarring of some of the glomeruli,
this condition may result from another disease or occur for no known reason
SIGNS AND SYMPTOMS.

Usually glomerulonephritis may present like nephrotic or nephritic syndrome, symptoms include;
 Proteinuria.
 Red blood cell casts.
 Oliguria.
 Hypertension.
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 Generalised edema.
 Headache.
 Nausea with/out vomiting.
 Abdominal pain.
 Hyperlipidemia.
 Hematuria.
 Hypoalbuminemia.

 Urinalysis; a urine sample is tested for amount of proteins to check for Hyperproteinuria. RBC.
 Blood samples; done to check for protein in blood, albumin levels and lipids.
 MRI, CT Scan and Abdominal ultrasound, a 12 lead ECG.
 Serum for electrolyte balance especially, BUN, Creatinine level.
 CBC or blood culture to isolate invading microorganism.
 Antihypertensive agents like Angiotensin Converting enzyme inhibitors (ACEI) like Captopril,
Enalapril, Isradipil to control Hypertension.
 Diuretics like Furosemide to reduce edema.
 Anti cholesterol agents to reduce risk of heart disease.
 Corticosteroids to reduce rate of inflammation like Prednisolone.
 Analgesics like Ibuprofen 400mg tds to control pain.
 Antibiotics like Phenoxymethylpenicillin-V to counteract underlying bacterial infection.
 Restrict salt intake to control hypertension.
 Thrombophilia: low molecular weight heparin (LMWH) may be appropriate for use as a
prophylactic in some circumstances.
NURSING INTERVENTIONS.
 Strictly admit patient in a warm made bed with adequate lighting, open adjacent windows to
enhance patients comfort.
 Position in sitting up or semi fowler position to increase venous return.
 Check the patient's vital signs and electrolyte values.
 Provide best rest during the acute phase.
 Perform passive range of motion exercises for the patient on bed rest.
 Allow the patient to resume normal activities gradually as symptoms subside.
 Consult the dietician about a diet high in calories and low in protein, sodium, potassium, and fluids.
 Protect the debilitated patient against secondary infection by providing good nutrition and hygienic
technique and preventing contact with infected people.
 Monitor intake and output and daily weight.
 Report peripheral edema or the formation of ascites.
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 Explain to the patient taking diuretics that he may experience orthostatic hypotension and dizziness
when he changes positions quickly.
 Provide emotional support for the patient and his family
 If the patient is scheduled for dialysis, explain the procedure fully.
COMPLICATIONS.
 Chronic renal failure.
 Malnutrition due to loss of proteins.
 Chronic glomerulonephritis.
 Anemia.
NEPHROTIC SYNDROME.
Nephrotic syndrome is a kidney disorder characterised by massive hyperprotenuria of more than 3g/dL in
24hours, hyperlipidemia, hypoalbuminemia and generalised edema.
PATHOPHYSIOLOGY.
The kidney glomerulus filters the blood that arrives at the kidney. It is formed of capillaries with small
pores that allow small molecules to pass through that have a molecular weight of less than 40,000 Daltons,
but not larger macromolecules such as proteins. In nephrotic syndrome, the glomeruli are affected by an
inflammation or a hyalinization that allows proteins such as albumin, antithrombin or the immunoglobulins
to pass through the cell membrane and appear in urine.
Albumin is the main protein in the blood that is able to maintain an oncotic pressure, which prevents the
leakage of fluid into the extracellular medium and the subsequent formation of edemas. As a response to
hypoproteinemia the liver commences a compensatory mechanism involving the synthesis of proteins, such
as alpha-2 macroglobulin and lipoproteins. An increase in the latter can cause the hyperlipidemia associated
with this syndrome.
CAUSES OF NEPHROTIC SYNDROME.

Nephrotic syndrome has many causes and may either be the result of a glomerular disease that can be either
limited to the kidney, called primary nephrotic syndrome (primary glomerulonephrosis), or a condition that
affects the kidney and other parts of the body, called secondary nephrotic syndrome
Primary Nephrotic syndrome causes;
 Minimal change disease (MCD): is the most common cause of nephrotic syndrome in children.
 Focal segmental glomerulosclerosis (FSGS): is the most common cause of nephrotic syndrome in
adults.
 Membranous glomerulonephritis (MGN): The inflammation of the glomerular membrane causes
increased leaking in the kidney.
 Membranoproliferative glomerulonephritis (MPGN): is the inflammation of the glomeruli along
with the deposit of antibodies in their membranes, which makes filtration difficult.
 Rapidly progressive glomerulonephritis (RPGN): A person's glomeruli are present in a crescent
moon shape.
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Secondary Nephrotic syndrome causes;

 Diabetic nephropathy.
 Systemic lupus erythematosus: this autoimmune disease can affect a number of organs, among them
the kidney.
 Sarcoidosis.
 Syphilis: kidney damage can occur during the secondary stage of this disease (between 2 and 8
weeks from onset).
 Hepatitis B: certain antigens present during hepatitis can accumulate in the kidneys and damage
them.
 Sjögren's syndrome.
 HIV: the virus's antigens provoke an obstruction in the glomerular capillary's lumen that alters
normal kidney function.
 Amyloidosis: the deposit of amyloid substances in the glomeruli modifying their shape and function.
 Multiple myeloma.
 Vasculitis: inflammation of the blood vessels at a glomerular level impedes the normal blood flow
and damages the kidney.
 Cancer: the invasion of the glomeruli by cancerous cells disturbs their normal functioning.
 Genetic disorders: congenital nephrotic syndrome is a rare genetic disorder in which the protein
nephrin, a component of the glomerular filtration barrier, is altered.
 Drugs like penicillin, captopril.
SIGNS AND SYMPTOMS.

 Cardinal features;
 Hyperprotenuria of more than 3.5g/dl in 24hours.
 Hyperlipidemia.
 Hypoalbuminemia of less than 2.5 g/dL, that exceeds the liver clearance level.
 Generalised edema (Anasarca).
 Hypercoagualability caused by a decrease in the levels of antithrombin III in the blood due to its loss
in urine.
 Other symptoms include the following;
 Puffiness around the eyes, characteristically in the morning.
 Pitting edema over the legs.
 Pleural effusion.
 Pulmonary edema.
 Ascites.
 Anasarca.
 Normotensive but hypertension (rarely) may also occur.
 Anaemia may be present due to transferrin loss.
 Dyspnea may be present due to pleural effusion.
 Erythrocyte sedimentation rate is increased due to increased fibrinogen & other plasma contents.
31
 Foamy or frothy urine, due to a lowering of the surface tension by the severe proteinuria.
 Rash associated with systemic lupus erythematosus.
 Neuropathy associated with diabetes.
 Muehrcke's nails or white lines (leukonychia).

 MRI, CT Scan and Abdominal ultrasound, a 12 lead ECG.
 Serum for electrolyte balance especially potassium, BUN, Creatinine level.
Aims;
To restore normal kidney function.
prophylactic in some circumstances,
 Admit patient in a warm made bed, with adequate lighting and adjacent windows opened to enhance
patients comfort.
 Monitor fluid and electrolyte balance. The nurse monitors the patient’s fluid and electrolyte levels
and physical indicators of potential complications during all phases of the disorder.
 Vital observations of TPR, Bp and record in patients file.
 Indwelling catheter to monitor urine output.
 Monitor fluid in and out put on fluid balance chart.
 Watch for nephrotoxic medications- statins, aminoglycosides
 Observe mental status.
 Ensure a low salt diet.
 Educate patient on renal failure.
 Nutritional therapy. A low protein diet is maintained to control and reduce wastes in the body.
32
 Semi fowlers position; The patient is placed in a semi fowler or sitting up position to reduce
pressure on the chest hence making breaking easier.
 Elevation of lower limbs; This is done to enhance venous return hence reduces oedema.
 Reducing metabolic rate. Bed rest is encouraged and fever and infection are prevented or treated
promptly.
 Promoting pulmonary function. The patient is assisted to turn, cough, and take deep breaths
frequently to prevent atelectasis and respiratory tract infection.
 Preventing infection. Asepsis is essential with invasive lines and catheters to minimize the risk of
infection and increased metabolism.
 Providing skin care. Bathing the patient with cool water, frequent turning, and keeping the skin
clean and well moisturized and keeping the fingernails trimmed to avoid excoriation are often
comforting and prevent skin breakdown.
 Provide safety measures. Patient with CNS involvement may be dizzy or confused.
 Auscultate heart and lung sounds to monitor state of lungs and breathing patterns.
 Evaluate presence of peripheral edema, vascular congestion and reports of dyspnea.
 Assess presence and degree of hypertension, monitor BP and note postural changes (sitting, lying,
standing).
 Assess activity level, response to activity.
COMPLICATIONS.
 Blood clot formation.
 Hypertension.
 Poor nutrition.
 Acute kidney failure.
 Chronic renal failure. Anemia.
NEPHRITIC SYNDROME.
Nephritic syndrome is a kidney disorder characterised by massive hematuria, oliguria, generalised edema
and hypertension. It often occurs in the glomerulus, where it is called glomerulonephritis.
PATHOPHYSIOLOGY.
The pathophysiology of nephritic syndrome is dependent on the underlying disease process, which can vary
depending on what condition the nephritic syndrome is secondary to. In all cases, however, the
inflammatory processes in the glomerulus cause the capillaries to swell and the pores between podocytes
become large enough that inappropriate contents in the blood plasma (i.e. red blood cells, protein, etc.) will
begin to spill into the urine. This causes a decrease in glomerular filtration rate (GFR) and, if left untreated
over time, will eventually produce uremic symptoms and retention of sodium and water in the body, leading
to both edema and hypertension.
CAUSES OF NEPHRITIC SYNDROME.

Children/adolescents;
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 IgA nephropathy; Most commonly diagnosed in children who recently had an upper respiratory tract
infection (URI). Symptoms typically present within 1–2 days of a non-specific URI
 Post-streptococcal glomerulonephritis (PSGN) - post-streptococcal glomerulonephritis (PSGN) most
often occurs in children who have recently had an upper respiratory infection (URI).
 Henoch Schönlein purpura (HSP).
 Hemolytic uremic syndrome - Most cases occur immediately following infectious diarrhea caused
by a specific type of E. coli (O157:H7).
Adults;
 Goodpasture syndrome - This is a rare autoimmune disease where auto antibodies are produced that
target the glomerular basement membrane in both the lungs and the kidneys.
 Systemic Lupus Erythematosus (SLE) - Better known as simply "Lupus", this autoimmune disease
can affect nearly every major system in the human body and the kidneys are no exception.
 Rapidly progressive glomerulonephritis - This is a syndrome of the kidney that is characterized by
rapid loss of kidney function (usually >50% decline in GFR within 3 months.
 Infective endocarditis.
 Cryoglobulinemia.
 Membranoproliferative glomerulonephritis (MPGN).
 Eosinophilic granulomatosis with polyangiitis.
 Microscopic polyangiitis.
 Granulomatosis with polyangiitis.
SIGNS AND SYMPTOMS.

Signs and symptoms that are consistent with nephritic syndrome include:
 Hematuria.
 Proteinuria of less than 3.5g/day. This doesn't exceed that of Nephrotic syndrome levels.
 Hypertension.
 Blurred vision.
 Azotemia (increased plasma Urea and Creatinine).
 Oliguria of less than 400 ml/day.
 Red blood cell casts.
 Pyuria.
DIFFERENCES BETWEEN NEPHROTIC AND NEPHRITIC SYNDROME.

SYMPTOMS NEPHROTIC NEPHRITIC
Red blood Cells Absent or less ++ Present or ++++
Proteinuria Above 3.5g/dl or ++++ Less proteins or ++
Onset Insidious or slow Abrupt onset
34
Oedema Severe or ++++ Moderate or ++
Blood pressure Usually normal High/raised
Hematuria With/without (+/-) Massive hematuria or ++++
Serum Albumin Low Normal with slight elevation
Urine casts Fatty casts RBC casts

 MRI, CT Scan and Abdominal ultrasound.
 Serum for electrolyte balance.
Aims;
prophylactic in some circumstances.

patients comfort.
35
 Restrict salt diet.

 Check BUN and creatinine levels.
 Nutritional therapy. A high protein diet is maintained.
promptly.
standing).
COMPLICATIONS.
 Acute renal failure.
 Heart failure.
 Anemia.
 Thromboembolism.
 Hypovolemic crisis.
ACUTE RENAL FAILURE (ARF).

Acute renal failure (ARF) or Acute kidney failure (AKF) is a condition characterised by a sudden
decrease in kidney functioning leading to accumulation of dangerous wastes like creatinine in the body.
This usually happens within hours to 7 days.
When your kidneys lose their filtering ability, dangerous levels of wastes may accumulate, and your blood's
chemical makeup may get out of balance. ARF or Acute kidney injury develops rapidly over a few hours or
a few days. Acute kidney failure is most common in people who are already hospitalized, particularly in
critically ill people who need intensive care.
CAUSES OF ARF.
36
The causes of ARF are classified by; Pre-renal, Intra-renal and Post-renal causes.
Pre-renal causes;
Diseases and conditions that may slow blood flow to the kidneys and lead to kidney failure include:
 Blood or Fluid loss.
 Blood pressure medications.
 Heart attack.
 Heart disease.
 Infection.
 Liver failure.
 Use of aspirin, ibuprofen, naproxen.
 Severe allergic reaction (Anaphylaxis).
 Severe Burns.
 Severe Dehydration.
Intra-renal causes;
These conditions and agents may damage the kidneys and lead to Acute kidney failure:
 Blood clots in the veins and arteries in and around the kidneys.
 Cholesterol deposits that block blood flow in the kidney.
 Glomerulonephritis.
 Hemolytic uremic syndrome, a condition that results from premature destruction of red blood cell.
 Infection.
 Lupus erythematosus.
 Medications like chemotherapy, antibiotics, medical dyes and zoledronic acid
 Multiple myeloma, a Cancer of the plasma cells
 Scleroderma.
 Thrombotic thrombocytopenic purpura.
 Toxins, such as alcohol, heavy metals and cocaine
 Vasculitis, an inflammation of blood vessels.
Post-renal causes;
Conditions that block the passage of urine out of the body and can lead to Acute kidney failure include:
 Bladder cancer.
 Blood clots in the urinary trac.
 Cervical cancer.
 Colon cancer.
 Enlarged prostate.
 Kidney stones.
 Nerve damage involving the nerves that control the bladder.
 Prostate cancer
RISK FACTORS OF ARF.

Conditions that can increase your risk of Acute kidney failure include:
 Being hospitalized, especially for a serious condition that requires intensive care
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 Advanced age, Peripheral artery disease.

 Diabetes, High blood pressure.
 Heart failure, Kidney diseases.
 Liver disease.
SIGNS AND SYMPTOMS OF ARF.

 Oliguria.
 Hypertension.
 Tachycardia.
 Drowsiness.
 Shortness of breath.
 Fatigue.
 Confusion.
 Nausea.
 Seizures or Coma in severe cases.
 Chest pain.
PHASES/STAGES OF ARF.
The phases/stages of ARF are Initial, Oliguric, Diuretic and Recovery phase.
1. Initial phase; This is a silent phase where changes take place without even patients notice.
2. Oliguric phase; Less urine production of less than 400ml/day and as it progresses, urine production
drops down to less than 100ml/day whereas in aneuric state, there is no urine at all.
3. Diuretic phase; Here, there is excessive urine production as kidneys carryout there function but
can't regulate urine output. It is this phase where a patient is at risk of developing acute dehydration.
4. Recovery phase; Here urine production comes back to normal as the kidneys can now regulate
urine output.
NOTE; The above stages/phases should NOT be confused with those of Chronic Renal failure (CRF/CKD).

ARF can be diagnosed if any one of the following is present (Specific Criteria);
 Increase in Serum Creatinine (SCr) by ≥0.3 mg/dl within 48 hours, or
 Increase in Serum creatinine (SCr) to ≥1.5 times baseline, which has occurred within the prior 7
days, or
 Urine volume < 0.5 ml/kg/h for 6 hours.
Urinalysis; a test done to examine micro/macroscopy of urine.
Uristic testing criteria;
 Ph; usually between 6.4 to 7.2
 Proteins; It should be absent but if present this may indicate pre-eclampsia, Glomerulonephritis,
Nephrotic and Nephritic syndrome.
 Bilirubin; if present this may indicate Malaria, Sickle Cell disease, Septicemia.
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 Glucose; this should be absent in urine. If present this may indicate diabetes.
 RBC; these should be absent but if present this may indicate Glomerulonephritis, Nephritic
syndrome.
 WBC; Indicates acute or chronic bacterial infection.
 Nitrates; indicates bacterial infection.
 Urobilinogen; this usually indicates obstructive jaundice.
 Specific Gravity; usually between 1.010 to 1.030. If its low may indicate an active infection or
diabetes.
 Ketones; If present this may indicate diabetes or DKA due to excessive breakdown of fats to form
energy.
 Blood culture to isolate invading microorganism.
 The 24hour urine testing; The urine may be analyzed for protein and waste products (urea nitrogen
and creatinine).
 Glomerular Filtration Rate; is a standard means of expressing overall kidney function. As kidney
disease progresses, GFR falls.
 Blood samples to check for Urea and creatinine.
 Abdominal ultrasound, MRI, CT Scan.
 A kidney biopsy.
 Cation-exchange resins or Kayexalate can reduce elevated potassium levels.
 Antibiotics like Phenoxymethylpenicillin-V given Qid.
 Antiinflammatory drugs like prednisolone to reduce rate of inflammation.
 IV dextrose 50%, insulin, and calcium replacement may be administered to shift potassium back into
cells.
 Diuretic agents like Furosemide are often administered to control edema.
Aims;
 Nutritional therapy. Caloric requirements are met with high-carbohydrate meals, because
carbohydrates have a protein-sparing effect; foods and fluids containing potassium or phosphorus
are restricted.
 After diuretic phase, the patient is placed on a high-protein and high-calorie diet.
39
promptly.
COMPLICATIONS OF ARF.
 Chronic renal failure.
 Hypertension.
 Septicemia.
 Muscle weakness.
 Pulmonary Oedema.
CHRONIC RENAL FAILURE (CRF/CKD).

Chronic renal failure (CRF) or Chronic Kidney Disease (CKD) is a kidney disorder characterised by
gradual loss of kidney function that usually takes months to years.
When Chronic kidney disease reaches an advanced stage, dangerous levels of Fluid, electrolytes and wastes
can build up in your body. In the early stages of Chronic kidney disease, you may have few signs or
symptoms. Chronic kidney disease may not become apparent until your kidney function is significantly
impaired.
CAUSES OF CKD.
Diseases and conditions that commonly cause Chronic kidney disease include:
 Diabetes Mellitus type 1 and 2.
 Hypertension.
 Glomerulonephritis.
 Interstitial nephritis.
 Polycystic kidney disease.
 Prolonged obstruction of the urinary tract, from conditions such as enlarged prostate, Kidney stones
and some Cancers
 Vesicoureteral reflux.
 Pyelonephritis.
40
SIGNS AND SYMPTOMS OF CKD.

 Signs and symptoms of kidney disease may include:
 Nausea and Vomiting.
 Fatigue and weakness.
 Sleep problems.
 Changes in urine output.
 Decreased mental sharpness.
 Muscle twitches and cramps.
 Hiccups.
 Persistent itching.
 Chest pain.
 Shortness of breath when fluid builds up in the lungs
 Hypertension that's difficult to control.
STAGES OF CKD.
Stage 1; GFR of 90ml/1.73m2 and above.
Stage 2; GFR of 60 to 89ml/1.73m2
Stage 3a; GFR of 45 to 63ml/1.73m2
Stage 3b; GFR of 30 to 44ml/1.73m2
Stage 4; GFR of 15 to 29ml/1.73m2
Stage 5; GFR of less than 15ml/1.73m2. This is the end stage and dialysis or kidney transplant is opted.

 Blood culture to isolate invading microorganism.
 CBC to check underlying infection.
 The 24hour urine testing; The urine may be analyzed for protein and waste products (urea nitrogen
and creatinine).
 Glomerular Filtration Rate; is a standard means of expressing overall kidney function. As kidney
disease progresses, GFR falls.
 Blood samples to check for Urea and creatinine.
 Abdominal ultrasound, MRI, CT Scan.
 A kidney biopsy.
The three levels of albuminuria include albumin-creatinine ratio (ACR)
A1: ACR less than 30 mg/gm (less than 3.4 mg/mmol)
A2: ACR 30 to 299 mg/gm (3.4 to 34 mg/mmol)
A3: ACR greater than 300 mg/gm (greater than 34 mg/mmol).
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Treatment is usually conservative as there is no cure for CKD, at some point in treatment even control of
symptoms like hypertension doesn't slow down the condition.
 Blood transfusion or Erythropoetin in cases of severe anemia.
 Calcium and Vitamin D supplements to control osteoporosis or bone loss.
 Antibiotics like Phenoxymethylpenicillin-V to control underlying bacterial infection.
 Antiinflammatory drugs like Prednisolone to control rate of inflammation.
 A low protein diet to control wastes in the body, this reduces kidney workload.
 Dialysis; this is done in case the kidneys can't do their work anymore. Tubes are inserted through the
peritoneum to filter wastes as your kidneys do.
 Kidney transplant; This is the last form of treatment as a new kidney is transplanted and the diseased
kidney is removed.
patients comfort.
 Monitor potassium levels.
 Ensure a low salt diet.
 Check BUN and creatinine levels.
 Nutritional therapy. A low protein diet is maintained to control and reduce wastes in the body.
promptly.
42
standing).
PATIENTS CONSIDERATION.
 Drug adherence.
 Cease or stop alcohol consumption.
 Stop cigarette smoking.
 Weight control.
 Control and manage hypertension.
 Review date.
COMPLICATIONS.
 Impotence.
 Decreased immune response.
 End stage kidney disease.
 Liver failure.
 Heart failure.
 Pulmonary edema.
 Hyperkalemia.
 Chronic anemia.
 Confusion and personality changes.
CONDITIONS AFFECTING THE NERVOUS

SYSTEM.
GENERAL SIGNS AND SYMPTOMS OF CNS CONDITIONS.
 Persistent or sudden onset of a headache
 A headache that changes.
 Loss of feeling or tingling.
 Weakness or loss of muscle strength.
 Loss of sight or double vision.
 Memory loss.
43
 Impaired mental ability.

 Lack of coordination.
 Muscle rigidity.
 Tremors and seizures.
 Back pain which radiates to the feet, toes, or other parts of the body.
 Muscle wasting and slurred speech.
 New language impairment (expression or comprehension).
MENINGITIS.
Meningitis is a neural condition characterised by an inflammation of the membranes (meninges)
surrounding the brain and spinal cord. Most cases of Meningitis in the U.S. are caused by a viral infection,
but bacterial and fungal infections also can lead to Meningitis. Depending on the cause of the infection,
Meningitis can get better on its own in a couple of weeks or it can be a life-threatening emergency requiring
urgent antibiotic treatment.
CAUSES OF MENINGITIS.
Bacterial Meningitis;
 Streptococcus Pneumoniae.
 Neisseria meningitidis.
 Haemophilus Influenzae.
 Listeria monocytogenes.
Viral Meningitis;
 Herpes simplex virus.
 HIV.
 Mumps.
 West Nile virus.
Fungal Meningitis;
 Cryptococcal Meningitis.
Other Meningitis causes;
 Chemical reactions.
 Drug Allergies.
 Some types of Cancer.
 Inflammatory diseases such as Sarcoidosis.
RISK FACTORS TO MENINGITIS.

 Compromised immune system. Factors that may compromise your immune system — including
AIDS, alcoholism, Diabetes.
 Pregnancy. If you're pregnant, you're at increased risk of contracting Listeriosis.
 Age. Most cases of viral Meningitis occur in children younger than age 5.
 Skipping vaccinations.
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SIGNS AND SYMPTOMS.

 Headache in about 90% of patients.
 Neck stiffness.
 Sudden high fever.
 Altered mental status or confusion.
 Drowsiness.
 Skin rash (meningococcal meningitis).
 Photophobia.
 Phonophobia (loud noise intolerance).
 Bulging fontanelle in infants.
 Irritability.
 Excessive sleepiness.
 Poor feeding.
 Positive Kernig's sign or Brudziński sign.
 Seizures.
 Fixed pupils.

 Blood culture test to identify invading microorganism.
 Blood for CBC.
 Spinal tapping for culture.
 Brain CT Scan.
 Brain MRI to view meninges.
Aims;
Viral Meningitis;
 Bed rest.
 Plenty of Fluids.
 Pain medications to help reduce Fever and relieve body aches.
Bacterial Meningitis;
 Broad spectrum antibiotics like Ceftriaxone 50mg/kg od is given.
 Ampicillin 50mg/kg qid or Gentamycin 3-7mg/kg od for weeks.
 Corticosteroids like Dexamethasone, Hydrocortisone 100-200mg bd to reduce brain swelling.
Fungal Meningitis;
 Amphotericin B in D5% 500ml tds is given. Protect drip from light.
 IV Fluconazole 400-800mg bd for weeks.
45
NOTE: To prevent kidney failure, infuse about 4L (4000ml) of Normal Saline before and after
administration of Amphotericin B.

 Where possible, raise the head of the bed greater than 30 degrees and maintain a neutral alignment.
 Maintain peripheral intravenous (IV) access and escalate loss of IV access to medical staff
immediately
 A quiet, dimly lit room can reduce agitation, especially in children and young people experiencing
photophobia and/or phonophobia.
 Reduce tactile handling of the child.
 Ensure adequate analgesia.
 Enteral feeds should be withheld in children with a reduced level of consciousness, vomiting or
having frequent convulsions.
 Children who are drinking well should have intravenous fluids run slowly to keep cannula patent.
 Blood sampling should continue 6-12hrly, until serum Na+ level is within normal ranges and stable.
 In infants, head circumference should be measured daily as Increased head circumference indicates
increased intra-cranial pressure.
COMPLICATIONS.
 Hearing loss.
 Memory difficulty.
 Learning disabilities.
 Brain damage.
 Gait problems.
 Seizures.
 Kidney failure.
 Shock.
PREVENTION OF MENINGITIS.
 Wash your hands. Careful hand-washing is important to avoiding exposure to infectious agents.
 Stay healthy. Maintain your immune system by getting enough rest, exercising regularly, and eating
a healthy diet.
 When you need to cough or sneeze, be sure to cover your mouth and nose.
 Haemophilus Influenzae type b (Hib) vaccine.
 Pneumococcal conjugate vaccine (PCV7).
 Meningococcal conjugate vaccine (MCV4).
 Haemophilus Influenzae type b and Neisseria meningitidis serogroups C and Y vaccine (Hib-
MenCY).
ENCEPHALITIS.
46
Encephalitis is a neural condition characterised by the inflammation of the brain tissue.

Many cases of encephalitis result in only mild Flu-like symptoms or even no symptoms. Severe cases of
encephalitis, while relatively rare, can be life-threatening. Because the course of any single case of
encephalitis can be unpredictable, it's important to get a timely diagnosis and treatment.
CAUSES OF ENCEPHALITIS.
An infection may result in one of two conditions affecting the brain:
Primary encephalitis; occurs when a virus or other infectious agent directly infects the brain. The infection
may be concentrated in one area or widespread. A primary infection may be a reactivation of a virus that
had been inactive (latent) after a previous illness. Viruses include;
 Herpes simplex virus. There are two types of herpes simplex virus (HSV). Either type can cause
encephalitis, HSV type 1 and 2.
 Epstein-Barr virus, which commonly causes infectious Mononucleosis.
 Varicella-zoster.
 Poliovirus.
 Coxsackievirus.
 Mosquito-borne viruses like Arboviruses or arthropod-borne viruses.
 Tick-borne viruses like the Powassan virus.
 Rabies virus.
 Childhood conditions like Measles, Mumps, Rubella viruses.
Secondary (postinfectious) encephalitis is a faulty immune system reaction in response to an infection
elsewhere in the body.
 Age; usually common in children and elderly.
 Immune suppression due to underlying infection like HIV/AIDS.
SIGNS AND SYMPTOMS.

 Headache.
 Fever.
 Aches in muscles or joints.
 Fatigue or weakness.
 Confusion.
 Agitation.
 Hallucinations.
 Seizures.
 Loss of sensation or paralysis in certain areas of the face or body.
 Muscle weakness.
 Double vision.
 Perception of foul smells, such as burned meat or rotten eggs.
 Problems with speech or hearing.
 Loss of consciousness
47
In children;
 Bulging in the soft spots (fontanels) of the skull in infants.
 Body stiffness.
 Inconsolable crying.
 Poor feeding or not waking for a feeding.
 Irritability.

 Lumbar puncture for CSF analysis.
 Blood culture to isolate invading microorganism.
 CBC for eosinophilia.
 Electroencephalogram.
 Brain tissue biopsy.
 Brain MRI.
 Brain CT Scan.
 C-Reactive Protein to check for inflammation.
Aims;
Incase of Viral Encephalitis;

Cases of encephalitis due to certain viruses usually require intravenous antiviral treatments.
 Acyclovir 400mg tds for weeks.
 Ganciclovir.
 Foscarnet.
Antibiotics include;
 Ceftriaxone 50mg/kg od as prescribed.
 Ciprofloxacin 500mg bd for weeks or as prescribed.
Other measures include;
 Bed rest
 Plenty of Fluids
 Anti-inflammatory drugs such as acetaminophen, ibuprofen and naproxen sodium.
 Anticonvulsant medications, such as phenytoin, to stop or prevent seizures.
 Anti-inflammatory drugs, such as corticosteroids, to help reduce swelling and pressure within the
skull.
 Breathing assistance, as well as careful monitoring of breathing and heart function.
 Intravenous Fluids to ensure proper hydration and appropriate levels of essential minerals.
48
 Psychotherapy to learn coping strategies and new behavioral skills to improve Mood disorders or
address personality changes.
 Speech therapy to relearn muscle control and coordination to produce speech.
 Occupational therapy to develop everyday skills.
 Physical therapy to improve strength, flexibility, balance, motor coordination and mobility.
COMPLICATIONS.
 Personality changes.
 Memory problems.
 Paralysis.
 Hearing or vision defects.
 Speech impairments.
PREVENTION OF ENCEPHALITIS.
 Always assist children with the use of mosquito repellent.
 Spray on clothing and exposed skin.
 Apply the repellent when outdoors to lessen the risk of inhaling the repellent.
 Spray repellent on your hands and then apply it to your child's face. Take care around the eyes and
ears.
 Don't use repellent on the hands of young children who may put their hands in their mouths.
 Wash treated skin with soap and water when you come indoors.
 Get rid of water sources outside your home.
 Dress to protect yourself.
CEREBRAL VASCULAR ACCIDENT(STROKE).

Cerebral Vascular Accident (CVA) or Stroke is a medical condition in which poor blood flow to the
brain causes cell death.
TYPES OF STROKE.
Ischemic stroke;
In an ischemic stroke, blood supply to part of the brain is decreased, leading to dysfunction of the brain
tissue in that area. There are four reasons why this might happen:
 Thrombosis (obstruction of a blood vessel by a blood clot).
 Embolism (obstruction due to an embolus from elsewhere in the body),
 Systemic hypoperfusion (general decrease in blood supply like during a shock)
 Cerebral venous sinus thrombosis.
Hemorrhagic stroke;
There are two main types of hemorrhagic stroke namely;
49
 Intracerebral hemorrhage, which is basically bleeding within the brain itself due to either
intraparenchymal hemorrhage or intraventricular hemorrhage.
 Subarachnoid hemorrhage, which is basically bleeding that occurs outside of the brain tissue but still
within the skull.
Hemorrhagic strokes may occur on the background of alterations to the blood vessels in the brain, such as;
 Cerebral amyloid angiopathy.
 Cerebral arteriovenous malformation.
 Intracranial aneurysm.
CAUSES OF STROKE.
Causes of stroke can be distinguished between high and low-risk:
High risk:
 Atrial fibrillation.
 Pulmonary embolism.
 Shock.
 Cerebral venous sinus thrombosis.
 Trauma.
 Bleeding disorders.
 Amyloid angiopathy.
 Illicit drug use like cocaine.
 Rheumatic heart disease.
 Artificial heart valves.
 Recent myocardial infarction.
 Chronic myocardial infarction together with ejection fraction less than 28%.
 Symptomatic congestive heart failure with ejection fraction less than 30%.
 Dilated cardiomyopathy.
 Infective endocarditis.
Low risk/potential:
 Calcification of the annulus (ring) of the mitral valve.
 Patent foramen ovale.
 Atrial septal aneurysm.
 Left ventricular aneurysm without thrombus.
SIGNS AND SYMPTOMS.

 Sudden-onset face weakness.
 arm drift; thats if a person when asked to raise both arms, involuntarily lets one arm drift downward.
 Abnormal speech.
 Loss of consciousness.
 Headache.
 Vomiting.
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NOTE; A mnemonic to remember the warning signs of stroke is FAST (Facial droop, Arm weakness,
Speech difficulty, and Time to call emergency services.
Other symptoms include;
 Numbness.
 Reduction in sensory or vibratory sensation.
 Altered smell, taste, hearing, or vision.
 Ptosis and weakness of ocular muscles.
 Decreased reflexes like gag, swallow, pupil reactivity to light.
 Muscle weakness of the face.
 Balance problems and nystagmus.
 Altered breathing and heart rate.
 Innability to turn head to one side.
If the cerebral cortex is involved, can produce the following symptoms:
 Aphasia.
 Dysarthria.
 Apraxia.
 Visual field defect
 Memory deficits.
 Hemineglect (involvement of parietal lobe)
 Disorganized thinking, confusion, hypersexual gestures.
 Lack of insight.

Physical examination with neurological examination is key with the use of the FAST mnemonic.
Imaging tests like;
 MRI scan, CTScan are done.
 An ultrasound study of the carotid arteries to detect carotid stenosis.
 An electrocardiogram (ECG) and echocardiogram to identify arrhythmias and resultant clots in the
heart.
 Holter monitor study to identify intermittent abnormal heart rhythms.
 Angiogram of the cerebral vasculature.
Aims;
 NG tube feeding since patient may fail to chew.
 Endotracheal Tube. There is a possibility of intubation to establish patent airway if necessary.
 Catheterisation to monitor fluid in and output.
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 Hemodynamic monitoring. Continuous hemodynamic monitoring should be implemented to avoid

an increase in blood pressure.
 Incase of Intracranial pressure, osmotic diuretics like Mannitol 20g is given.
Incase of Ischemic stroke;
 Control of hypertension or Diabetes if present.
 Aspirin is used to reduce the risk of stroke reoccurrence by thinning blood.
 Enoxaparin 80mg od given subcutaneously to breakdown clots in circulation.
 Mechanical thrombectomy this involves mechanical removal of the blood clot causing the ischemic
stroke.
Incase of hemorrhagic stroke;
 Require supportive care, including blood pressure control if required.
 People are monitored for changes in the level of consciousness, and their blood sugar and
oxygenation are kept at optimum levels.
 Endovascular surgery.
 Hemicraniectomy to reveal the site.
NOTE; Anticoagulants and antithrombotics can make bleeding worse and are generally discontinued in
the management of hemorrhagic stroke.

 Positioning. Position to prevent contractures, relieve pressure, attain good body alignment, and
prevent compressive neuropathies.
 Prevent flexion. Apply splint at night to prevent flexion of the affected extremity.
 Prevent adduction. Prevent adduction of the affected shoulder with a pillow placed in the axilla.
 Prevent edema. Elevate affected arm to prevent edema and fibrosis.
 Full range of motion. Provide full range of motion four or five times a day to maintain joint mobility.
 Prevent venous stasis. Exercise is helpful in preventing venous stasis, which may predispose the
patient to thrombosis and pulmonary embolus.
 Regain balance. Teach patient to maintain balance in a sitting position, then to balance while
standing and begin walking as soon as standing balance is achieved.
 Personal hygiene. Encourage personal hygiene activities as soon as the patient can sit up.
 Manage sensory difficulties. Approach patient with a decreased field of vision on the side where
visual perception is intact.
 Visit a speech therapist. Consult with a speech therapist to evaluate gag reflexes and assist in
teaching alternate swallowing techniques.
 Voiding pattern. Analyze voiding pattern and offer urinal or bedpan on patient’s voiding schedule.
 Be consistent in patient’s activities, schedule, routines, and repetitions.
 Assess skin. Frequently assess skin for signs of breakdown, with emphasis on bony areas and
dependent body parts.
COMPLICATIONS.
 Tissue ischemia.
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 Cardiac dysrhythmias.
PREVENTION OF STROKE.
 Adequate monitoring of hypertension.
 Adequate control of sugar levels.
 Helmets to avoid head banging.
 Take Aspirin in those with a previous history of stroke.
 Exercise to reduce weight gain.
 Statins to reduce bad cholesterol like Atovastatin.
UNCONSCIOUSNESS/COMA.
Unconsciousness is a state which occurs when the ability to maintain an awareness of self and environment
is lost. It involves a complete or near-complete lack of responsiveness to people and other environmental
stimulus.
A Coma is a prolonged state of unconsciousness. It occurs when a temporary or permanent disruption of the
brain’s function severely affects consciousness
CAUSES OF UNCONSCIOUSNESS.
Unconsciousness may occur as the result of the following;
 Traumatic brain injury.
 Brain hypoxia.
 Inhalation of carbondioxide which reduces oxygen to brain.
 Hypoglycemia due to excessive hunger.
 Cardiac arrest.
 Severe intoxication with drugs that depress the activity of the central nervous system like alcohol
and other hypnotic or sedative drugs.
 Severe fatigue.
 Prolonged standing in hot sunshine.
 Upon receiving shocking news.
 Severe pain.
 Anaesthesia.
 Severe dehydration.
 Head injury.
CAUSES OF A COMA.
 Traumatic brain injuries, such as those caused by traffic accidents or violent trauma.
 Stroke (reduced blood supply to the brain).
 Tumors in the brain or brainstem.
 Lack of oxygen to the brain after being rescued from drowning or from a heart attack
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 Unmanaged diabetes, which causes blood sugar levels to become too high (hyperglycemia) or too
low (hypoglycemia) and can lead to swelling in the brain
 Overdosing on drugs or alcohol.
 Carbon monoxide poisoning.
 Buildup of toxins in the body, such as ammonia, urea, or carbon dioxide.
 Heavy metal poisoning like lead.
 Infections, such as meningitis or encephalitis.
 Repeated seizures.
 Electrolyte imbalance.
SIGNS AND SYMPTOMS OF A COMA.

 Closed eyes.
 Unresponsiveness.
 Irregular breathing.
 No response of limbs, except for reflexes.
 No response to pain, except for reflexes.
SIGNS AND SYMPTOMS OF UNCONSCIOUSNESS.

Symptoms that may be associated with decreased consciousness include:
 Seizures.
 Loss of bowel or bladder function.
 Poor balance or gait.
 Falling.
 Difficulty walking.
 Fainting.
 Light headedness .
 Irregular heartbeat.
 Rapid pulse.
 Hypotension.
 Sweating.
 Fever.
 Weakness in the face, arms or legs.
TYPES AND LEVELS OF DECREASED CONSCIOUSNESS:

These are called types or levels of impaired consciousness, they include; Confusion, Disorientation,
Delirium, Lethargy, Stupor and Coma.
Confusion;
 Confusion is marked by the absence of clear thinking and may result in poor decision-making.
Disorientation;
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 Disorientation is the inability to understand how you relate to people, places, objects, and time. The
first stage of disorientation is usually around awareness of your current surroundings like; why
you’re in the hospital.
 The next stage is being disoriented with respect to time like years, months, days. This is followed by
disorientation with respect to place, which means you may not know where you are.
 Loss of short-term memory follows disorientation with respect to place. The most extreme form of
disorientation is when you lose the memory of who you are.
Delirium;
 If you’re delirious, your thoughts are confused and illogical. People who are delirious are often
disoriented. Their emotional responses range from fear to anger. People who are delirious are often
highly agitated as well.
Lethargy;
 Lethargy is a state of decreased consciousness that resembles drowsiness. If you’re lethargic, you
may not respond to stimulants such as the sound of an alarm clock or the presence of fire.
Stupor;
 Stupor is a deeper level of impaired consciousness in which it’s very difficult for you to respond to
any stimuli, except for pain.
Coma;
 Coma is the deepest level of impaired consciousness. If you’re in a coma, you can’t respond to any
stimulus, not even pain.
LEVELS OF AWARENESS IN COMA.

Persistent vegetative state.
 When someone is in a persistent vegetative state, they’re unaware of their surroundings and unable
to move voluntarily. This condition can sometimes last indefinitely, and when it does, it’s called a
permanent vegetative state.
Minimally conscious state.
 This state of consciousness sometimes occurs when someone comes out of a vegetative state. They
have limited signs of awareness and can occasionally respond to stimuli or requests like grab my
hand, but it’s hard for them to retain consciousness for long periods.
Brain death.
 This is different from a coma and is not reversible. The definition of brain death includes specific
criteria, such as a lack of certain reflexes. Several doctors will perform a medical examination to
determine if the brainstem and cerebrum are functioning.

Physical examination with use of glassgo coma scale is key.
Desired tests include;
 Urinalysis
 Blood count
 Thyroid and liver function
 Electrolyte levels
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 Blood sugar levels

 Carbon monoxide poisoning
 Drug overdose
 Alcohol overdose
 Infections of the nervous system
 Computerized tomography scans. CT scans use X-rays to create a detailed image of the brain.
 Magnetic resonance imaging (MRI). An MRI uses radio waves and magnets to view the brain.
 Electroencephalography (EEG). An EEG measures electrical activity inside the brain.
Aims;
To restore normal brain function.
 Avoid use of oral route due to risk of aspiration, maintain parenteral route till patient is awake.
 Intravenous Fluids like normal saline to stabilize blood pressure to prevent hypotension.
 Analgesics like Intramuscular Diclofenac 75mg stat.
 Antibiotics like Ceftriaxone 50mg/kg od as prescribed to counteract underlying bacterial infection.
 Dextrose 5% or 10% incase of hypoglycemia or alcohol intoxication.
 Incase the cause is not identified, antidotes are given basing on the clinical presentation of the
patient.
 Oxygen therapy to correct a low oxygen saturation to above 92%.
 2 hourly turning of the patient to prevent bed sores.
 Maintain a recovery or sitting up position to avoid pressure on airway.
 Intubation incase of severe obstruction.
 Suctioning to reduce airway secretions.
 Protecting the patient from falling off the bed.
 Maintaining fluid balance and managing nutritional needs.
 Maintaining skin integrity.
 Preventing urinary retention and incontinence by catheterization.
 Providing sensory stimulation
 Identifying Potential complications like respiratory Distress, Pneumonia, Aspiration, Bed Sores and
others.
POLIOMYELITIS(POLIO).
Poliomyelitis is a viral illness thats characterised by paralysis, difficulty breathing and sometimes death. If
you're a previously vaccinated adult who plans to travel to an area where Polio is occurring, you should
receive a booster dose of inactivated Poliovirus vaccine (IPV). Immunity after a booster dose lasts a lifetime.
CAUSES OF POLIOMYELITIS.
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 Polio virus is the only cause of Poliomyelitis which is transmitted from an infected person through
their fecal matter. Ingesting food or water contaminated with infected stool confers you the illness.
RISK FACTORS TO POLIO.

 Travel to an area where Polio is common or that has recently experienced an outbreak
 Living with or caring for someone who may be shedding Poliovirus
 A compromised immune system, such as occurs with HIV infection
 After tonsillectomy.
 Extreme stress or strenuous physical activity after being exposed to Poliovirus, both of which can
depress your immune system.
 Poor sanitation.
 Failure to wash hands after visiting the toilet.
 Eating unwashed fruits.
SIGNS AND SYMPTOMS OF POLIO.

The vast majority of people who are infected with the Poliovirus don't become sick and are never aware
they've been infected with Poli, symptoms base on the stage or phase you posses;
Nonparalytic Polio/Abortive polio;
Some people who develop symptoms from the Poliovirus contract nonparalytic Polio, a type of Polio that
doesn't lead to paralysis (abortive Polio). This usually causes the same mild, Flu-like signs and symptoms
typical of other viral illnesses.
Signs and symptoms, which generally last one to 10 days, include:
 Fever
 Sore throat
 Headache
 Vomiting
 Fatigue
 Back pain or stiffness
 Neck pain or stiffness
 Pain or stiffness in the arms or legs
 Muscle weakness or tenderness
 Meningitis
Paralytic Polio;
In rare cases, Poliovirus infection leads to paralytic Polio, the most serious form of the disease. Paralytic
Polio has several types, based on the part of your body that's affected. For example;
 Spinal cord (spinal Polio).
 Brainstem (bulbar Polio).
 If both, bulbospinal Polio.
Within a week, however, signs and symptoms specific to paralytic Polio appear, including:
 Loss of reflexes
 Severe muscle aches or weakness
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 Loose and floppy limbs (flaccid paralysis), often worse on one side of the body
 Post-polio syndrome
Post-polio syndrome;
Is a cluster of disabling signs and symptoms that affect some people several years, an average of 35 years
after they had Polio. Common signs and symptoms include:
 Progressive muscle or joint weakness and pain
 General fatigue and exhaustion after minimal activity
 Muscle atrophy
 Breathing or swallowing problems
 Sleep-related breathing disorders, such as Sleep apnea
 Decreased tolerance of cold temperatures
 Cognitive problems, such as concentration and memory difficulties
 Depression or mood swings.

A physical examination is usually performed with emphasis on neck stiffness and back, weakness of one
limb.
 A throat swab for culture.
 A blood culture to isolate invading microorganism.
 CSF analysis.
Aims;
NOTE; There is no cure for Poliomyelitis and so, preventive measures is opted for.
 Bed rest
 Pain relievers
 Portable ventilators to assist breathing
 Moderate exercise (physical therapy) to prevent deformity and loss of muscle function
 A nutritious diet.
CONDITIONS OF THE ENDOCRINE SYSTEM.

DIABETES MELLITUS.
Diabetes Mellitus is a chronic metabolic disorder characterised by persistent hyperglycemia for along
period of time.
TYPES OF DIABETES.
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Diabetes Mellitus type 1;

 This is an autoimmune disorder resulting from destruction of the beta cells in the pancreas known to
secret insulin. Also called Insulin dependent diabetes.
Diabetes Mellitus type 2;
 This is known as adult onset or noninsulin dependent Diabetes, is a chronic condition that affects the
way your body metabolizes glucose.
Prediabetes;
 This is called so because blood sugar levels range between 9-12mmol/dL but not classified as
Diabetes Mellitus. Incase the individual doesn't change his/her lifestyle, they later progress to DM
type 2.
Gestational diabetes;
 This happens during pregnancy and should subside immediately after labour. Incase blood suave
levels fail to drop, its classified as DM type 2.
Diabetes inspidus;
 Is a condition characterized by large amounts of dilute urine and increased thirst. The amount of
urine produced can be nearly 20 liters per day.
SIGNS AND SYMPTOMS OF DM TYPE 1 AND 2.

Some of the signs and symptoms of type 1 and Type 2 diabetes are:
 Polydipsia (Increased thirst).
 Polyuria (Frequent urination).
 Polyphagia (Extreme hunger).
 Unexplained weight loss in DM type 1.
 Obesity in DM type 2.
 Presence of ketones in the urine.
 Fatigue
 Irritability
 Blurred vision
 Slow-healing sores
 Frequent infections, such as gums or skin infections and vaginal infections.
CAUSES OF DM TYPE 1.
 The exact cause is unknown but its believed to arise from the autoimmune destruction of beta cells
in the pancreas known to secret insulin. This leaves the glucose unable to enter the cells and
multiplies within the circulation hence causing hyperglycemia.
RISK FACTORS TO DM TYPE 1.

 Family history.Your risk increases if a parent or sibling has Type 1 diabetes.
 Environmental factors. Circumstances such as exposure to a viral illness likely play some role in
Type 1 diabetes.
 The presence of auto antibodies. But not everyone who has these auto antibodies develops Diabetes.
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 Dietary factors. These include low vitamin D consumption, early exposure to cow's milk or cow's
milk formula, and exposure to cereals before 4 months of age. None of these factors has been shown
to directly cause Type 1 diabetes.
 Geography. Certain countries, such as Finland and Sweden, have higher rates of Type 1 diabetes.
CAUSES OF PREDIABETES AND DM TYPE 2.

 In Prediabetes which can lead to Type 2 diabetes, your cells become resistant to the action of insulin,
and your pancreas is unable to make enough insulin to overcome this resistance. Instead of moving
into your cells where it's needed for energy, sugar builds up in your bloodstream.
RISK FACTORS TO DM TYPE 2, PREDIABETES AND GESTATIONAL DIABETES.

 Weight. The more fatty tissue you have, the more resistant your cells become to insulin.
 Inactivity. Physical activity helps you control your weight, uses up glucose as energy and makes
your cells more sensitive to insulin.
 Family history. Your risk increases if a parent or sibling has Type 2 diabetes.
 Race.Including blacks, Hispanics, American Indians and Asian-Americans are at higher risk.
 Age. Your risk increases as you get older.
 Gestational diabetes. If you developed Gestational diabetes when you were pregnant, your risk of
developing Prediabetes and Type 2 diabetes later increases.
 Polycystic ovary syndrome. increases the risk of Diabetes.
 High blood pressure. Having blood pressure over 140/90 mm Hg is linked to an increased risk of
Type 2 diabetes.
 Abnormal cholesterol and triglyceride levels. If you have low levels of high-density lipoprotein
(HDL) "good cholesterol" your risk of Type 2 diabetes is higher.

 Glycated hemoglobin (HbA1C) test, a level of 6.5% or higher on two separate tests indicates that
you have Diabetes.
 Random blood sugar test; a reading of 11.1mmol/L indicates Diabetes.
 Fasting blood sugar test; a reading of 5.6 mmol/L is normal. A reading of 5.6 to 6.9mmol/L is
considered Prediabetes.
 Oral glucose tolerance test.
 Urinalysis for ketones.
 Blood cultures.
 Blood Urea Nitrogen levels.
 Blood for thyroid stimulating hormone levels and T3,T4.
 Thyroid scans.
 Insulin therapy; many types of insulin are available, including rapid acting insulin, long-acting
insulin and intermediate options.
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 Antidiabetics like Biguanides including Metformin as the first line drug can be given 500-1g od or
bd depending on the response.
 Sulfonylureas like Glibenclamide 5mg od can be given.
 Monitoring of glucose levels is key.
 Pancreas transplant surgery.
 Cholesterol reducing agents like Statins including Atovastatin, Simvastatin.
 Weight control.
 Exercise to prevent a sedentary lifestyle.
 Avoid cigarettes or alcohol consumption.
 Educate about home glucose monitoring. Discuss glucose monitoring at home with the patient
according to individual parameters to identify and manage glucose variations.
 Review factors in glucose instability. Review client’s common situations that contribute to glucose
instability because there are multiple factors that can play a role at any time like missing meals,
infection, or other illnesses.
 Encourage client to read labels. The client must choose foods described as having a low glycemic
index, higher fiber, and low-fat content.
 Discuss how client’s antidiabetic medications work. Educate client on the functions of his or her
medications because there are combinations of drugs that work in different ways with different
blood glucose control and side effects.
 Check viability of insulin. Emphasize the importance of checking expiration dates of medications,
inspecting insulin for cloudiness if it is normally clear, and monitoring proper storage and
preparation because these affect insulin absorbability.
 Review type of insulin used. Note the type of insulin to be administered together with the method of
delivery and time of administration. This affects timing of effects and provides clues to potential
timing of glucose instability.
 Check injection sites periodically. Insulin absorption can vary day to day in healthy sites and is less
absorbable in lipohypertrophic tissues.
THE DIABETIC FOOD/PLATE.

Proteins; these take Quarter ¼ a plate.
 Meat, Milk.
 Fish.
 Eggs.
 Beans.
 Soya, Cowpeas
Vegetables; these take Half ½ a plate.
 Cabagge.
 Sukuma wiki.
 Avocados.
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 Watermelon.
 Carrots.
 Oranges and lemons.
Carbohydrates; these take Quarter ¼ a plate.
 Millet.
 Sorghum.
 Sweet potatoes. Wheat.
 Cassava. Ground nuts.
 Yams. Irish potatoes.
 Maize, Rice.
COMPLICATIONS.
 Diabetic ketoacidosis (DKA).
 Coronary artery disease with Angina.
 Heart attack.
 Diabetic nephropathy.
 Diabetic retinopathy.
 Diabetic foot syndrome leading to amputation.
 Stroke.
 Pre-eclampsia and eclampsia.
 Atherosclerosis.
 Subsequent gestational diabetes in the next pregnancies.
PREVENTION OF DIABETES.
 Adequate monitoring of glucose levels is key.
 Lose weight if obese.
 Avoid or cease cigarette smoking.
 Control or stop alcohol consumption.
 Exercise regularly.
 Avoid stress.
 Always treat viral infections.
 Avoid fatty foods.
 Do periodic check up of glucose levels.
THYROTOXICOSIS.
Thyrotoxicosis is an endocrine disorder that occurs due to massive production of thyroid hormones (T3 and
T4) of any cause by the thyroid gland.
CAUSES OF THYROTOXICOSIS.
 Thyroiditis.
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 Graves disease; an autoimmune disease usually, the most common cause with 50–80% of cases.
 Toxic thyroid adenoma.
 Toxic multinodular goiter.
 Oral consumption of excess thyroid hormone tablets.
 Postpartum thyroiditis occurs in about 7% of women during the year after they give birth.
 Hypersecretion of thyroid stimulating hormone.
 Excess iodine consumption.
 Amiodarone, an antiarrhythmic drug.
SIGNS AND SYMPTOMS OF THYROTOXICOSIS.

 Palpitations
 Wight loss.
 Exophthalmia.
 Diarrhea.
 Anxiety.
 Heat intolerance.
 Hair loss.
 Muscle aches,.
 Weakness.
 Fatigue.
 Hyperactivity.
 Irritability.
 High blood sugar.
 Excessive urination.
 Excessive thirst
 Delirium.
 Tremor.
 Pretibial myxedema (in Graves' disease).
 Emotional lability.
 Panic attacks.
 Inability to concentrate.
 Memory problems may also occur.
 Psychosis.

 Blood sample for TSH levels.
 serum for T3,T4 levels.
 Thyroid scan.
 MRI and CTScan can be done.
 Thyroid scintigraphy to differentiate hyperthyroidism from Thyroiditis.
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Drugs that inhibit the production of thyroid hormones like;
 Carbimazole
 Methimazole 15-40mg tds initially.
 Propylthiouracil 300-450mg tds initially, maintain at 100-150mg tds for months.
 Beta blockers to control palpitations like propranolol, Atenolol.
 Reduce iodine intake.

 Administer dextrose intravenous fluids as ordered to correct fluid and glucose deficits.
 Carefully assess the patient for heart failure or pulmonary edema.
 Dopamine may be used to support blood pressure.
 Provide supplemental oxygen as ordered to help meet increased metabolic demands.
 Once the patient is hemodynamically stable, provide pulmonary hygiene to reduce pulmonary
complications.
 If the patient is in heart failure, typical pharmacologic agents for treatment of heart failure may also
be indicated.
 Reduce oxygen demands by decreasing anxiety, reduce fever, decrease pain, and limit visitors if
necessary.
 Anticipate aggressive treatment of precipitating factor.
 Institute pressure ulcer strategies.
COMPLICATIONS.
 Heart failure.
 Liver failure.
 Kidney stones.
 Brain injury.
 Dehydration.
ALL ABOUT SPECIFIC NURSING CARE/INTERVENTIONS A

NURSE SHOULD KNOW.
By definition; Nursing interventions are actions a nurse takes to implement their patient care plan,
including any treatments, procedures, or teaching moments intended to improve the patient's comfort and
health.
CATEGORIES OF NURSING INTERVENTIONS.

The NI are grouped into 3 (three) categories;
Independent: A nurse can perform independent interventions on their own without assistance from other
medical personnel like; checking/taking vital observations.
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Dependent: Some actions require instructions or input from a doctor, such as prescribing new medication.
A nurse cannot initiate dependent interventions alone.
Interdependent: Also called Collaborative or interdependent interventions involve team members across
disciplines. In certain cases, such as during post operative care, the patient’s recovery plan may require a
prescription medication from a doctor, feeding assistance from a nurse, and treatment by a physical
therapist or occupational therapist.
PURPOSE OF NURSING CARE/INTERVENTIONS.

Reaching health goals; Many nursing interventions help patients reach their wellness and recovery goals.
A primary responsibility for nurses is to aid in treatment plans for a patient to improve their health or
quality of life. Examples of nursing interventions that serve this purpose are administering medications,
changing bandages and helping patients stay hydrated.
Educating patients; Educating patients, families and their caregivers about the patient's condition and
treatment plan is important to a successful recovery. Nurses provide instruction or education on how to
support patients at home, manage their condition and perform treatment plan after discharge.
Promoting safety; Nursing interventions also promote patient safety by taking preventive measures, such
as helping patients change their bed positions to prevent injuries.
Offering support; Nursing interventions may also offer emotional support and comfort to a patient or their
family. Nurses can recommend resources for therapy to handle stress.
TYPES/CLASSIFICATIONS OF NURSING INTERVENTIONS.

There are 7 (Seven) types/classifications of nursing interventions.
Community nursing; these are nursing practices that can affect many people at once. These are public
health initiatives that seek to educate or encourage a community to take part in a healthy activity. An
example would be a health fair, which is set up at schools to teach children, but they invite the public to
attend and learn from health experts.
Family nursing; these are programs to help family members support one another. An example is infant
care for new parents when nurses teach parents how to bathe, feed, swaddle and perform other tasks for
their baby
Health system nursing; these are often interdependent interventions that promote patient safety and
involve a team of medical professionals. An example is a procedure to reduce infection, which can include
interventions such as administering antibiotics, bathing the patient and changing wound dressings.
Safety nursing; these are tasks and nursing procedures for the overall well-being of patients, such as
educating patients and families on postoperative care. These are also interventions of taking precautions to
prevent injury and protect the patient while they are in the hospital or long-term care facility. Bed
positioning, alarms and railings and orienting a patient to their room are all examples of safety nursing
interventions.
Physiological basic nursing; these are simple nursing procedures that assist patients with their physical
health. This can include exercise and assessments of the patient's blood pressure or temperature. Triage
nurses in the ER need to be experts in physiological nursing interventions because many of these
interventions involve assessing a patient and treating physical aliments.
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Physiological complex nursing; these are procedures that comprise smaller tasks to promote or assist a
patient with their physical health. Providing IV fluids can be a physiological complex nursing intervention
because it involves inserting the IV needle, administering medication and monitoring the patient.
Behavioral nursing; these are tasks that help patients learn methods to change behaviors. Nurses use
behavioral analysis to assess a patient when performing this type of intervention.
EXAMPLES OF GENERAL NURSING CARE/INTERVENTIONS.

These are daily nursing interventions you will perform and perfect throughout your career as a nurse, these
are done everyday and to all patients. They include;
Pain control:
 Ensuring that the patient is comfortable and monitoring their intake of analgesics if available.
Vital observations;
 These are crucial to each and every patient as they allow a nurse to monitor patients response to
treatment and disease prognosis. In case of any emergency, vital observations are checked first.
Position changes:
 Promoting a change of the patient’s resting position to prevent bedsores, this is usually done at every
after 2 hours.
Active listening:
 Listening to the patient and repeating back information so they feel heard. This enhances a safe
working environment and cooperation.
Cluster care:
 Informing other nurses and care team members of the patient’s needs each shift to help consolidate
trips and avoid frequent traffic in the patient’s room
Fall prevention:
 Educating the patient, generally someone who is elderly or recovering post-surgery, of instructions
to avoid the risk of fall and injury. This maybe attained by raising side rails of the bed.
Fluid intake:
 This means helping patients stay hydrated, which is important for their physical health. This may
either be intravenous or oral intake.
Mobility therapy:
 Nurses may teach patients exercises they can practice to increase mobility. Mobility therapy also
includes moving patients' limbs, especially in cases of paralysis, to prevent muscles from atrophy.
Assistive device therapy:
 A common task for nurses is to help patients with the use of assistive devices, such as a wheelchair
or insulin pens. They teach patients how to help themselves at home after a diagnosis.
Sleep pattern control:
 Assisting patients with healthy sleeping habits is important to help them recover. Sleep pattern
control may involve monitoring or education. For example for a patient with breathing problems, a
sitting up, Semi fowlers or recovery positions maybe helpful.
Nutritious diet;
66
 An exclusive intervention is to provide a nutritious diet to the patient since drugs are less effective
without diet. Through proteins and carbohydrates the body heals and energy is regained. Its
therefore crucial for a nurse to assess nutritional requirements for their patients.
Promoting selfcare;
 A nurse should allow their patients to carryout simple tasks themselves like combing, brushing,
applying Vaseline in order to establish selfcare. This boosts the patient's prognosis.
Patent flow of IV needle and line;
 A crucial intervention of a nurse is to make sure the IV line and needle are patent to allow for easy
transfusion especially in cases of emergency. This patency prevents over pricking of the patient
which is usually painful and uncomfortable.
Encourage out of bed activity;
 Out of bed activities are helpful to the patient as they allow for fresh air, relieve stress and allow
patient to get oriented about the place. This is also helpful along side physiotherapy.
Deep Vein Thrombosis (DVT) and pressure sore prophylaxis;
 For all bed ridden or debilitating patients, adequate DVT prophylaxis and pressure sores treatment
should be provided to prone areas like scapular region, elbows, buttocks, heels.
Drug compliance;
 Adequate provision of patients treatment on time is key to patients health and mandatory to a nurse.
This enables maintenance of stable drug doses hence quickens healing and prevents relapses.
Hygiene;
 This involves bed birth, oral care, change of soiled linens. Hygiene should be maintained by a nurse
as it reduces infections to the patient and promotes comfort.
Emotional support;
 As patients are worried about their disease state, a nurse should provide emotional support and
obtain confidence from the patient. This enhances comfort and allows boosts trust.
Wound dressing;
 This is done to those patients with ulcers. Aseptic technique should be improvised to prevent cross
infections and quicken healing.
Infection control;
 Adequate hand washing and provision of PPE where applicable should be done as this reduces risk
of infection and promotes a safe working environment for nurse and patient.
Funeral arrangement:
 Incase the patient passes away, nurses can assist families with funeral arrangements when a member
passes away while in their care. This is a good example of family nursing intervention.
Advice on discharge;
 This is crucial for a nurse to offer advice or information to any patient upon their discharge, this may
involve drug adherence, prevention of the disease, review date or return date.
END.
67

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CONDITIONS AFFECTING THE DIGESTIVE

SIGNS AND SYMPTOMS.

TESTS AND DIAGNOSIS.

SIGNS AND SYMPTOMS.

TESTS AND DIAGNOSIS.

SPECIFIC NURSING INTERVENTIONS.

PEPTIC ULCER DISEASE (PUD).

SIGNS AND SYMPTOMS.

 Nausea and vomiting.

TESTS AND DIAGNOSIS.

SPECIFIC NURSING INTERVENTIONS.

2. Hepatic causes (hepatocellular);

3. Post hepatic causes (obstructive);

RISK FACTORS TO JAUNDICE.

SIGNS AND SYMPTOMS OF JAUNDICE.

TESTS AND DIAGNOSIS.

SPECIFIC NURSING INTERVENTIONS.

SIGNS AND SYMPTOMS OF HEPATITIS.

 The non specific symptoms typically fade away by this time.

TESTS AND DIAGNOSIS.

SPECIFIC NURSING INTERVENTIONS.

LIVER CIRRHOSIS (LC).

CAUSES OF LIVER CIRRHOSIS.

SIGNS AND SYMPTOMS OF LC.

TESTS AND DIAGNOSIS.

To prevent further complications.

SPECIFIC NURSING INTERVENTIONS.

 Change patient’s position frequently.

 Orient to time, place, and procedures to minimize agitation.

 Kinking of bile duct.

SIGNS AND SYMPTOMS.

TESTS AND DIAGNOSIS.

SPECIFIC NURSING INTERVENTIONS.

CONDITIONS AFFECTING THE URINARY

SIGNS AND SYMPTOMS OF URETHRITIS.

TESTS AND DIAGNOSIS.

SIGNS AND SYMPTOMS.

 A burning sensation when urinating.

TESTS AND DIAGNOSIS.

RISK FACTORS OF PYELONEPHRITIS.

SIGNS AND SYMPTOMS.

TESTS AND DIAGNOSIS.

LIFESTYLE CHANGES/ PATIENTS CONSIDERATIONS.

SIGNS AND SYMPTOMS.

TESTS AND DIAGNOSIS.

CAUSES OF NEPHROTIC SYNDROME.

Secondary Nephrotic syndrome causes;

SIGNS AND SYMPTOMS.

TESTS AND DIAGNOSIS.

CAUSES OF NEPHRITIC SYNDROME.

SIGNS AND SYMPTOMS.

DIFFERENCES BETWEEN NEPHROTIC AND NEPHRITIC SYNDROME.

Red blood Cells Absent or less ++ Present or ++++

Proteinuria Above 3.5g/dl or ++++ Less proteins or ++

Onset Insidious or slow Abrupt onset

Oedema Severe or ++++ Moderate or ++

Blood pressure Usually normal High/raised

Hematuria With/without (+/-) Massive hematuria or ++++

Serum Albumin Low Normal with slight elevation

Urine casts Fatty casts RBC casts

TESTS AND DIAGNOSIS.

SPECIFIC NURSING INTERVENTIONS.