3RD Satchot of 2nd Smester

Question 1

explain Hypersecretory Syndrome , DF , provking factors,causes , Complaints ,Mechanism of the pain ,duadenal vs gastric , Inspection and Palpation , signes

Answer 1

-DF : This syndrome is caused by an increase in the
production of hydrochloric acid and pepsin
activity,
-Provking factors :
* Disturbance of diet (dry eating, very hot, spicy
* food, etc.)
* Irregular nutrition
* Alcohol abuse, smoking
* Helicobacter pylori
-Causes :
1. Chronic gastritis with increased secretory activity of the stomach
* 2. Peptic ulcer with localization in the duodenum and antrum (pyloric) stomach
* 3. Duodenitis
-Complaints :
* heartburn after eating,
* sour belching;
* vomiting acidic masses, facilitating the patient’s condition;
* increased appetite;
-Mechansim of pain :
* Spastic:
* definite localization - in the epigastric region to the right of the midline and in the right hypochondrium
* irradiation in the back
* paroxysmal
-Dudenal Vs gastric :
1- Dudenal :
Pain is relave by meal ,occures 2-3h after meal
,Dark stool (malena )
2-Gastric :
Pain increasced by meal , occuers after 30 min of meal , vomating occures
- Inspection and Palpation :
* Forced position of the body (pose of the “embryo”)
* soreness in the epigastric region
-Sgins : Fibrogastroduodenoscopy
* Signs of hypersecretion (erosion, ulcers, fibrin, pinpoint hemorrhages)

Question 2

explain Hyposecretory syndrome , DF ,Causes ,complains ,Mechanism of the pain , Inspection and palpation ,sings

Answer 2

-DF : This syndrome is caused by a decrease in gastric secretion and is combined with a decrease in the motor activity of the stomach
-Causes :
* 1. Atrophic gastritis
* 2. Gastric ulcer
* 3. Cancer of the stomach
-Complains :
* decreased appetite;
* belching after meals
* intolerance to fatty and coarse foods, milk and dairy products;
* nausea;
* diarrhea
-mechnasim of pain :
* associated with distended stomach.
* occur after eating, sometimes immediately, often after 30-40 minutes (early pain)
* low-intensity, dull, aching pains or only a feeling of heaviness in the epigastric region, sometimes to the left of the midline, without clear localization and without irradiation. The pain disappears usually after 2-3 hours.
- Inspection and palpation :
* Weight loss
* Signs of anemia due to malabsorption of iron, vitamin deficiency
* Diffuse tenderness in epigastrium
-Sings :Fibrogastroduodenoscopy
* Hypo- / atrophy of the gastric mucosa

Question 3

explain Abdominal pain syndrome , Spastic pain ,Distension pain ,Vascular pain ,Peritoneal pain,Acute Abdomen Syndrome

Answer 3

1-Spastic pain :
-DF : due to spasm of the smooth muscles of the gastrointestinal tract
-Charectarstic : sharp, paroxysmal with a clear localization
-Causes : gastric colic (hypersecretion), intestinal colic, biliary colic
————————-
2-Distension pain :
-DF: associated with hypomotor dyskinesia of smooth muscles and hollow organ distension
-Charectarstic : dull pains, non-intense, without clear localization
-Causes : flatulence, hyposecretory syndrome
—————————-
3-Vascular pain
-DF : associated with a violation of the blood supply
to the abdominal cavity, as a result of this,
ischemia and necrosis develop sudden onset,
very intense, progressive,
-Casuses :mesenteric thrombosis, embolism, ischemic disease of the digestive system
————————–
4-Peritoneal pain :
-DF :based on tension of the capsule or visceral sheet of the peritoneum
-Charetrstic :peritoneal pain occurs gradually or suddenly (with perforation), increases, intense, accompanied by tension of the abdominal wall,
-Causes :peritonitis due to inflammation of the organs
(appendicitis, acute cholecystitis, acute pancreatitis) and perforation of the stomach and intestines
——————————–
5-Acute Abdomen Syndrome :
* Acute surgical pathology:
* Perforated ulcer of the stomach and duodenum
* Acute appendicitis
* Acute cholecystitis
* Acute pancreatitis
* Bowel obstruction

Question 4

explain Gastrointestinal (GI) bleeding : DF , Casues ,Signs ,types,Physical examination ,Testing ,

Answer 4

-DF :can originate anywhere from the mouth to the anus and can be overt or occult.
-Casuses :
1-Upper tract :
* Duodenal ulcer (20–30%)
* Gastric or duodenal erosions (20–30%)
* Varices (15–20%)
* Gastric ulcer (10–20%)
2-Lower GI tract:
* Anal fissures
* Angiodysplasia (vascular ectasia)
* Colitis: Radiation, ischemic, infectious
* Colonic carcinoma
* Colonic polyps
-sings :Red flags! Several findings suggest hypovolemia or
hemorrhagic shock:
* Syncope
* Hypotension
* Pallor
* Sweating
* Tachycardia
-Types :
1.Hematemesis
2.Hematochezia
3.Melena
-Physical examination :
* indicators of shock or hypovolemia: tachycardia,
* tachypnea, * pallor, * diaphoresis, * oliguria,
-Testing :
* Complete blood count (CBC), coagulation profile,
* Upper endoscopy for suspected upper GI bleeding
* Colonoscopy for lower GI bleeding
* Flexible sigmoidoscopy and anoscopy
* Digital rectal examination

Question 5

explain Hematemesis

Answer 5

-DF :is vomiting of red blood and indicates upper GI bleeding, usually from a peptic ulcer, vascular lesion, or varix
-Charectarstic : Coffee-ground emesis is vomiting of
dark brown, granular material that
resembles coffee grounds
-Pathoginsis :It results from upper GI bleeding that has slowed or stopped, with conversion of red hemoglobin to brown hematin by gastric acid.

Question 6

explain Melena

Answer 6

-DF : is black, tarry stool and typically indicates upper GI
bleeding, but bleeding from a source in the small bowel
-Location : ileocecal valve
-NB! : Black stool that does not contain occult blood may result
from ingestion of iron, bismuth, or various foods and
should not be mistaken for melena

Question 7

explain Hematochezia

Answer 7

-DF : is the passage of gross blood ( braight or dark red ) from the rectum and usually indicates lower GI bleeding but may result from vigorous upper GI bleeding with rapid transit of blood through the intestines.

Question 8

explain Gastric emptying delay syndrome
(pyloric stenosis) , DF , Casuse , pathoginisis ,Compilanis ,Objective data ,diagnosis

Answer 8

-DF : Acquired pyloric stenosis is a narrowing of the
pyloric (output) section of the stomach, which
is a consequence of stomach diseases in
adults
-Casues : peptic ulcer or tumer in the ploric orfecis
-Pathoginisis :
1-Initial stage- the muscles of the stomach are still able to overcome the obstacle that arises, and the food lingers in the stomach for a short time.
2-Progressive stage - food lingers for a longer time, the stomach grows in size, and atony of its muscles develops. As a result, food ceases to pass into the duodenum almost completely.
-Complains:
1.a feeling of fullness in the upper abdomen after eating, periodically occurring vomiting,
2.In advanced cases, the patient’s condition becomes severe, vomiting may be absent, as a result of a large loss of fluid, convulsions develop.
-Objactive data :
1.enlarged contours of the stomach in the upper abdomen
2.↓ body weight up to cachexia
3.convulsions
-Diagnosis ;
1.X-ray
* Gastroptosis
* Stomach is enlarged, stretched, hypotonic,
* Evacuation is dramatically slowed down
* On an empty stomach contains a lot of liquid and food masses
2.Fibrogastroduodenoscopy : * Pylorosthenosis

Question 9

explain Malabsorption syndrome , DF , Causes , symptoms and sings ,Diagnosis

Answer 9

-DF :refers to a number of disorders in which
nutrients from food are not absorbed properly
in the small intestine.
-Causes ;
* Gastrectomy, Intestinal resection
* Biliary obstruction and cholestasis
* Cirrhosis
* Chronic pancreatitis, Pancreatic cancer, Pancreatic resection
* Cystic fibrosis
-Symptoms and sings :
* Chronic diarrhea
* Steatorrhea—fatty stool, the hall mark of malabsorption—occurs when > 7 g/day of fat are excreted.
* Steatorrhea causes foul-smelling, pale, bulky, and greasy stools.
* Abdominal pain, distention
* Increased flatulence
* Lose weight
* Other symptoms result from nutritional deficiencies.
* Anemia
* Amenorrhea
-Diagnosis :
1. Blood tests (complete blood count, ferritin, vitamin B12, folate, calcium, albumin, cholesterol, prothrombin time)
2. Stool fat testing to confirm malabsorption
3.Contrast x-rays

Question 10

explain Syndrome of exocrine pancreatic insufficiency : DF ,Causes , clinical picture ,Dyspeptic syndrome ,Pancreatic diarrheas and malabsorption and
maldigestion syndromes Diagnosis

Answer 10

-DF : is a condition characterized by deficiency of the exocrine pancreatic enzymes, resulting in the inability to digest food properly, or maldigestion. Pancreatic insufficiency causes malabsorption if > 90% of function is lost
-Causes :
* Chronic pancreatitis (the most common cause of EPI)
* Acute pancreatitis
* Cystic fibrosis
* Obstructions of the pancreatic duct (eg, from pancreatic cancer)
-Clinical picture :
* The exocrine pancreas produces three main types of enzymes: amylase, protease, and lipase.
* When lipase and protease secretions are reduced to < 10% of normal, the patient develops malabsorption characterized by steatorrhea, the passing of greasy stools. In severe cases, undernutrition, weight loss, and malabsorption of fat-soluble vitamins (A, D, E, and K) may also occur.
-Dyspeptic syndrome : * increased salivation, * air or eaten food
eructation, * nausea, vomiting, * loss of appetite, * fatty food intolerance, flatulence * weight loss
-Pancreatic diarrheas and malabsorption and maldigestion syndromes :
* are characteristic of severe pancreatic exocrine insufficiency,
* diarrhea are caused by alterations of pancreatic enzymes release and intestinal digestion,
* excretion of abnormal quantities of fat with the feces owing to reduced absorption of fat by the intestine.
-Diagnosis :
1.X Ray
2. Ultra sound

Question 11

explain the Hemolytic prehepatic jaundice , DF , mechansim ,Causes , clinical picture ,Laboratory changes

Answer 11

-Df : Hemolytic (suprahepatic or prehepatic) - high blood levels of unconjugated (indirect) bilirubin
-mechansim :Increased formation of unconjugated (indirect) bilirubin from the RBC
-Causes :
1.sickle anemia
2.Malaria
3.thalssmia
-clincial picture :
* Skin color - lemon yellow.
* The color of the urine is not changed or darker than usual.
* Stool color normal or dark
* Hepatomegaly
* Splenomegaly
-Laboratory changes:
* ↑ indirect bilirubin in the blood,
* ↑ urobilin in the urine,
* ↑ Increased stercobilin in feces
* Bilirubin is absent in the urine

Question 12

explain Hepatic cell (parenchymal) jaundice , DF ,michansim , cuases , clincial picture ,Laboratory changes

Answer 12

-DF : Hepatic cell (parenchymal) - increased blood levels of both indirect and direct bilirubin.
-Mechansim : Hepatocyte damage
-Causes :
-hepatitis,
-cirhosis,
-liver cancer
-alcohol;
- viruses;
- medicines;
-Clincial picture :
* Skin color - yellow
* Urine is darker than usual
* The stool color is not changed or discolored.
* Hepatomegaly
* Splenomegaly
-Laboratory changes:
* ↑ direct (to a greater extent) and indirect bilirubin in the blood,
* ↑ urobilin in the urine
* urine bilirubin is determined
* stercobilin in feces is normal or ↓(reduced)

Question 13

explain Mechanical jaundice , DF , mechansim , Casues ,Clinical picture , Laboratory changes

Answer 13

-DF :Mechanical (subhepatic or post-hepatic, obstructive) - high blood levels of conjugated (direct) bilirubin
-Mechansim ;Biliary obstruction
-Causes :
-Cholelithiasis
-Pancreatic head tumor
-Bile duct cancer
-Clinical picture :
* Skin Color: Dark Yellow
* Itchy skin
* The color of urine is very dark (like beer)
* Feces - discolored
-Laboratory changes :
* ↑ Direct bilirubin in the blood,
* ↑ bilirubin in urine
* Urobilin is absent in urine
* Stercobilin in feces is absen

Question 14

explain Portal Hypertension , DF , Types amd causes of each , Mixed form of portal hypertension syndrome ,Manifestations , General examination ,Diagnostics

Answer 14

-DF : this is an increase in pressure in the portal vein system caused by a disturbance of blood flow in the portal vessels, hepatic veins, and the inferior vena cava
-Types :
1.Posthepatic form of Portal Hypertension : caused by difficulty in the outflow of blood from the hepatic veins. It is manifested by the development of:
-ascites,
-pain in the liver,
-significant hepatomegaly with a relatively small increase in the spleen.
2.intahepatic : the most common cause of portal hypertension
(80% of all cases). Obstruction of blood flow is in the liver itself.
* Persistent dyspeptic syndrome,
* flatulence, * diarrhea, * weight loss.
* In the later stages - splenomegaly with hypersplenism,
* varicose veins with possible bleeding * ascites.
3.Prehepatic form of Portal Hypertension : occurs with occlusion of the portal or splenic veins.
* liver is usually not enlarged
* splenomegaly with hypersplenism without bleeding and ascites,
* less frequent repeated bleeding from the veins of the esophagus, followed by ascites
-Mixed form of portal hypertension syndrome :is associated with the
development of portal vein thrombosis in patients with cirrhosis
-Manifestations:
1. Ascites
2. Signs of collateral circulation: - varicose veins of the esophagus;;
- “medusa head”;
3. Splenomegaly, hypersplenism
4.Bleeding from varicose veins
-General examination :
1.Drum sticks
2.Ascitits
3.Medusa viens
-Diagnostics:
* Ultrasound examination of the liver
* Esophagogastroduodenoscopy

Question 15

explain Hepatic insufficiency , DF , types and casuses of each , main indicator on liver faliur

Answer 15

-DF ;impaired liver function due to acute or chronic damage to hepatocytes
-Types :
1.Chronic :* hepatitis, * cirrhosis, * tumors, * heart failure;
2.Acute: * drug damage, * poisons, * sepsis, * shock,
–Main indicators of hepatic cell failure: :
* 1. Disturbance of the protein-synthetic function of the liver
* 2. Disturbance of the carbohydrate function of the liver
* 3. Disturbance of lipid function of the liver
* 4. Disturbance liver pigment function
* 5. Disturbance of the neutralizing function of the liver

Question 16

explain hepatic encephalopathy Df , Clinical signs

Answer 16

-DF ;is defined as a brain dysfunction caused by liver insufficiency and/or portal-systemic blood shunting
-Clinical sings :
* 1. Mental disturbance: sleep disturbance in the form of inversion, the appearance of nightmare dreams, memory, intelligence are gradually
reduced, dementia develops.
* 2. Movement disorders: small tremor of the fingers resembles “flapping the wings of a bird”, bradykinesia, increased tendon reflexes, impaired
coordination.
* 3. Change of the encephalogram (EEG): inconstant and weakly expressed.

Question 17

explain the hepatic coma DF , clinical sings

Answer 17

-DF ;If the underlying cause of liver disease isn’t treated, liver function deteriorates, and toxins continue to build. Some people with advanced hepatic encephalopathy lose consciousness and go into a hepatic coma
-Clincial sings :
1. Developing coma: drowsiness, marked disorientation in space, clapping tremor of the fingers, eyelids, ataxia, dysarthria, reflexes are increased, handwriting disorder, fever,
* 2. Sopor, pronounced disorientation in space.
* 3. Hepatic coma (deep coma):
* hepatic odor from the mouth,
* jaundice

Question 18

explain Hepatolienal syndrome , DF ,Causes ,Clinical features ,Hypersplenism(DF , Causes ,Clinical picture , Laboratory Chnages )

Answer 18

-DF ;combined lesion of the liver and spleen, due to their close connection
with the portal vein system, the generality of innervation, and the
pathways of lymphatic drainage.
-Causes :diffuse liver damage,circulatory disorders in the portal vein system, accumulation diseases (amyloidosis), systemic blood diseases, sepsis, heart failure
-Clinical picture:
1 - with portal hypertension - a large spleen (there may be more liver), hypersplenism;
2- with congestive heart failure - spleen is slightly increased, hypersplenism is absent;
3 - infiltrative lesions can be equally expressed in both organs (with sepsis), mainly in the spleen (with hemoblastosis),
—Hypersplenism :
-DF :accompanies a significant increase in the spleen and is manifested by an increase in its normal function to remove destroyed blood cells.
-Causes :all forms of portal hypertension, granulomatosis with enlarged spleen
-Clinical picture :
*can be asymptomatic,
* sometimes manifested by a feeling of heaviness in the left hypochondrium;
* palpation - pain and enlargement of the spleen,
* hemorrhagic syndrome.
-Laboratory changes:
* anemia,
* leukopenia,
* thrombocytopenia.

Question 19

explain the Renal colic syndrom , DF , Mechanism of pain , Clinical manifestations , Characteristic signs of renal colic , Diagnosis ,Complications

Answer 19

–DF : is manifested by pain due to obstruction of the upper urinary tract (calyces of the kidney, pelvis and ureters). More common in men.
-The main reason is obstruction of the urinary system:
* urolithiasis,
* calculous pyelonephritis.
–Mechanism of pain:
* overflow of the pyelocaliceal system with urine above the site of occlusion,
* increased pressure in the renal pelvis,
* impaired blood circulation in the kidney
* muscle spasm
* local inflammation and swelling at the site of obstruction
—Clinical manifestations:
1-A sudden attack of pain in the lumbar region, provoked by physical exertion
2-Nature of pain: acute
* Spreading: to the entire corresponding half of the abdomen, radiating to the inguinal region.
* The patient is constantly changing position.
* Duration: from several hours to a day
* Accompanied by: nausea, vomiting, frequent painful urination, stool retention, muscle tension of the anterior abdominal wall, increased blood pressure.
–Characteristic signs of renal colic :
* expectoration concrement (usually after a pain attack)
* hematuria (often macrohematuria) due to trauma to
the stone and a sharp increase in pressure inside the
pelvis.
–Diagnosis :
* X-ray of the abdomen
* Intravenous urography IVU
* Ultrasound
* urinalysis
–Complications:
* acute and chronic pyelonephritis,
* hydronephrosis,
* acute renal failure (with ureteral occlusion - obstructive anuria),
* chronic renal failure (associated with the terminal stage of chronic pyelonephritis)

Question 20

explain the Renal hypertension syndrome , DF , detected in,Patogenesis ,Pathogenesis,Complications of malignant arterial hypertension

Answer 20

–DF : Hypertensive syndrome is a pathological condition,
which is based on an increase in blood pressure due
to pathology of the kidneys or renal vessels
–Hypertensive syndrome may be detected in:
* 1) parenchymal (acute and chronic glomerulonephritis
chronic pyelonephritis, diabetic nephropathy, nephrocarcinoma, polycystic kidney disease;
* 2) Vasorenal hypertension renal artery stenosis
atherosclerosis of the vessels of the kidneys, aortoarteritis
–Patogenesis:
* vasorenal or renoparenchymal genesis of hypertension
- retention of Na and water due to activation of reninangiotensin-aldosteron system (RAAS) and depression
of prostaglandin-callecrein system function
–Manifestations :
* depends on degree of BP elevation and damage of cardiovascular system. Changes in urine appears before increase of BP.
* headache, blurred vision, pain in the heart, shortness of breath
* ↑BP (especially high and persistent diastolic pressure),
* left ventricular hypertrophy
* pronounced retinopathy
* systolic murmur during auscultation of the abdomen at the site of projection of the renal arteries,
* signs of narrowing of the renal vessel during aortography
–Complications of malignant arterial hypertension:
* loss of vision (blindness),
* hypertensive encephalopathy,
* heart failure

Question 21

explain Nephrotic syndrome : DF , Etiology,Clinical manifestations ,Complications, diagnosis

Answer 21

–DF : is a complex of symptoms, including:
* Massive proteinuria (>3.5 g/24 h)
* Hypoalbuminemia (< 35 g/l)
* Disproteinemia (hyper-α2- globulinemia)
* Dislipidemia (cholesterol increase)
* Edema (due to ↓of serum oncotic pressure and retention of Na )
-NB! : Arterial hypertension and hematuria are
not characteristic signs of nephrotic
syndrome!
–Etiology :
1. Primary glomerulonephritis (acute and chronic)
2. Kidney damage in the following conditions:
* a) infectious and parasitic diseases - chronic viral hepatitis; malaria, schistosomiasis; infectious endocarditis;
* b) systemic diseases - systemic lupus erythematosus, hemorrhagic vasculitis; rheumatoid arthritis;
* c) amyloidosis;
* d) diabetes mellitus;
* e) tumors - paraneoplastic nephrotic syndrome with
bronchogenic cancer, cancer of the parenchyma of the kidney,
stomach, colon, malignant lymphoma;
3. Drug damage to the kidneys: antiepileptic drugs, gold
preparations, mercury, D-penicillamine, antibiotics).
–Clinical manifestations
* The leading clinical sign of nephrotic syndrome is edema,
from moderate to degree anasarca with dropsy cavities
(ascites, hydrothorax, hydropericardium).
* skin - pale, dry, atrophic.
–Complications of nephrotic syndrome:
* 1. infectious (bacterial, viral, fungal), due to the low
content of immunoglobulins lost with urine proteins.
frequent pneumonia, pleurisy.
* 2. vascular - peripheral phlebo- and
arteriothromboses (pulmonary embolism, thrombosis
of the arteries of the kidney with the development of
necrosis of its parenchyma, strokes, myocardial
infarction), in connection with severe
hypercoagulation.
* In patients with NS due to severe dyslipidemia, the
development of atherosclerosis occurs earlier.
Hyperlipidemia is a factor in the progression of
glomerular damage and leads to glomerulosclerosis
–Diagnosis :
* 1. Urinalysis - high relative density (may
* reach 1,030-1,050), contains hyaline, granular,
* epithelial and waxy cylinders, white blood cells.
* 2. Immunological studies
* 3. Kidney biopsy
* 4. Blood test – hyperfibrinogenemia.

Question 22

explain Nephritic (acute nephritic) syndrome , DF ,Causes,Manifestations,Complications

Answer 22

–DF :
* this symptom complex is characterized by inflammation of the glomerular apparatus of the kidneys.
* The occurrence of acute nephritic syndrome is most
characteristic of acute post-streptococcal nephritis (especially
in children and young men), 2-3 weeks after the infection
–Causes:
* 1. Infections
* 1.1. Acute post-streptococcal glomerulonephritis
* 1.2. Other glomerulonephritis associated with
* infection: - bacterial: infectious endocarditis, sepsis; -viral: hepatitis B and C, - parasitic: malaria,btoxoplasmosis
* 2. Primary chronic glomerulonephritis
* 3. Systemic diseases:
* - systemic lupus erythematosus;
* - systemic vasculitis;
—Manifestations:
* 1. Edema (periorbital puffiness, ankle edema from latent edema to anasarca)
* 2. Urinary syndrome (brown or cola-coloured urine, proteinuria <3.5 g / day).
* 3. Arterial hypertension
* 4. Oliguria
–Complications:
1. Renal eclampsia:
* - a significant increase in blood pressure;
* - cramps;
* - visual impairment;
* - coma
2. Acute left ventricular failure:
* cardiac asthma, pulmonary edema
3. Acute renal failure

Question 23

explain Acute renal failure ,DF ,Etiology ,Clinical manifestations ,treatment ,

Answer 23

–df :
* a sudden impairment of renal function with a delay
in the elimination of nitrogen metabolism products
from the body and an upset of water-electrolyte and
acid-alkaline balance.
* result of severe acute renal blood flow damage,
glomerular filtration, and tubular reabsorption,
usually occurring simultaneously
–Eiology :3 groups of acute renal failure
1-Prerenal:
Sudden and severe drop in blood pressure (shock) or interruption of blood flow to the kidneys from severe injury or illness
2-Intrarenal:
Direct damage to the kidneys by inflammation, toxins, drugs, infection, or reduced blood supply
3-Postrenal:
Sudden obstruction of urine flow due to enlarged prostate, kidney stones, bladder tumor, or injury
—Clinical manifestations
1. The period of action of the etiological factor - symptoms of
the disease leading to acute renal failure
2. Oligoanuric period (2-3 weeks):
* - decrease in diuresis, edema, weight gain, nausea, vomiting;
* - pulmonary edema, edema brain, uremic coma;
* - increased creatinine, potassium, urea in the blood serum,
hyperhydration, metabolic acidosis
3. Reduction period (5-10 days):
* - polyuria;
* - dehydration, decreased concentration, potassium, sodium
* 4. Recovery (6-12 months)
–treatment : Hemodialysis * Treatment of acute and chronic renal failure using the artificial kidney apparatus.

Question 24

explain Chronic renal failure , DF,Etiology ,clinincal manfsitation ,Diagnostic criteria of chronic renal failure,Classification of chronic renal failure

Answer 24

–df :The clinical condition resulting from chronic
derangement and insufficiency of renal excretory and
regulatory function (uremia)
–Eitology :
* glomerulonephritis - 57.4%;
* pyelonephritis - 13.9%;
* polycystic kidney disease - 11.1%;
* diabetic nephrosclerosis - 5.1%;
* congenital and hereditary lesions of the kidneys - 3.8%;
* systemic diseases –2.2%;
* arterial hypertension - 2.0%;
* amyloidosis - 0.9%
–clinincal manfsitation :
1-Cardiovascular: High blood pressure, increased heart rate
2-Immune: Increased risk of infection
3-Musculoskeletal :Renal osteodystrophy, decreased calcium, vitamin D impairment, hyperparathyroidism, pathological fractures
4-Neurological: Peripheral neuropathy, restless legs, change in level of consciousness,
5-Gastrointestinal: Anorexia, nausea, vomiting, halitosis, metallic taste in mouth, bleeding in gastrointestinal tract
Renal: Decreased urine output, azotemia, proteinuria, hernaturia, hyperuricemia
6-Respiratory : Increased respiratory rate, Kussmaul respirations, crackles, decreased Po2
–Diagnosis :
* - a decrease in glomerular filtration rate, an increase
in the concentration of creatinine, urea, potassium,
uric acid;
* - a decrease in the specific gravity of urine (isostenuria, hypostenuria);
* - reduction in hemoglobin, erythropoietin
production;
* - metabolic acidosis;
* - violation of phosphorus-calcium metabolism;
* - reduction in the size of the kidneys and parenchyma
–Classification of chronic renal failure:
is based on the grade of severity and characteristic clinical
manifestations.
* Mild: GFR is 30—50 ml/min.
* Moderate: GFR is 10—30 ml/min.
— anemia;
— hypertension;
— osteodystrophy.
* Grave: GFR is 5—10 ml/min.
— nausea;
— anorexia;
— pruritus.
* Terminal (end-stage): GFR is < 5 ml/min.
— pericarditis; — pulmonary edema; — coma.