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CM test 2 > GI, heptaobilary and pancrease, renal > Flashcards

GI, heptaobilary and pancrease, renal Flashcards

1
Q 
atresia
 definition
 associated with (4)
 results in...
 manifested by...
A
  1. atretic - having an occluded lumen of developmental origin of esophagus
  2. may be associated with other GI abnormalities, vertebral defects, or cardiovascular malformations with atretic portion usually located at the level of tracheal bifurcation.
  3. This usually results in tracheo-esophageal fistula
  4. It is manifested by salivation, and coughing from reflux of gastric acid.
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2
Q

hiatia hernia
def
is it symptomatic?

A
  1. protrusion of portion of stomach above diaphragm
  2. this is really bad because of low pH of stomach which is usually blocked by
  3. most are asymptomatic but 10% of pts will have heartburn- from insufficiency of sphincter- gastric fluids go up
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3
Q 
sliding hernia
 def
 why its important
A
  1. when traction from scarred or congenitally shortened esophagus pulls the cardia (upper portion becuase its close to heart) of the stomach through the esophageal hiatus
  2. this is important because similar symptoms of MI
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4
Q

rolling hernia (2)

A
  1. inherited abnormality
  2. occurs when portion of gastric fundus protrudes thru defect in esophageal hiatus (accentuated by intraabdominal pressure)
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5
Q 
achalasia
 characterized by
 etiology
 what happens
 clinical signs
A
  1. characterized by the failure of the gastroesophageal sphincter to relax
  2. unknown etiology (may be due to loss of ganglion cells in the plexus myentericus Auerbachi)
  3. Food is retained within the esophagus proximal to the gastroesophageal sphincter. The esophagus is dilated and the may become thinned or thickened from compensatory muscular hypertrophy.
  4. Clinically there is dysphagia, food regurgitation and aspiration pneumonia.
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6
Q

diverticula
what it is
2 possibly causes

A
  1. developmental or acquired outpouching of the esophagus wall.
    due to:
  2. increased intraluminal pressures (pulsion diverticula) occurring on the posterior wall proximal to the upper esophageal sphincter, in the mid esophagus, or immediately proximal to the gastroesophageal sphincter
  3. due to healing of inflammatory process external to the esophagus (traction diverticula) with fibrosis creating distortion.
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7
Q

esophageal varices
what it is
what it does (2)

A
  1. vascular disorder of the esophagus due to hepatic portal hypertension (from any cause, usually cirrhosis)
  2. diverts the normal portal venous flow into the azygous system of veins and esophageal veins.
  3. produces distended veins beneath the esophageal mucosa. They are generally asymptomatic until rupture occurs (when varices reach size greater than 5 mm in diameter) causing massive hematemesis.
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8
Q

reflux esophagitis
what it is
what it does to you (biology)
adenocarcinoma

A
  1. inflammatory reaction cause by esophageal injury due to regurgitation of gastric contents which may or may not be associated with hiatal hernia.
  2. Superficial epithelial necrosis, peptic ulcerations, and submucosal inflammation are present to varying degrees in the distal third of the esophagus leading to fibrosis and structures or replacement of squamous by columnar epithelium- Barrett esophagus. (this is metaplasia)
  3. Approximately 10% of patients will develop adenocarcinoma.
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9
Q 
Congenital pyloric stenosis
 what it is
 due to...
 who does it affect most
 how can it be acquired?
A
  1. narrowing of the pyloric canal (connects gut to intestine)
  2. due to hypertrophy of the circular muscle of the pylorus that may be palpated as a mass in the newborn also having projectile vomiting.
  3. This disorder is 4:1 predominant in males and it is the most common indication for abdominal surgery in the initial 6 months of life.
  4. Acquired forms of pyloric stenosis- postinflammatory scarring
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10
Q 
gastritis
 def 
 acute - what it is (normal and sciency def)
 what causes it (6 things)
 symptoms of acute gastritis
A
  1. in inflammatory disease that can be acute (erosive) or chronic (nonerosive)
    acute:
  2. stress ulcer- presence of focal necrosis and petechial hemorrhages of the mucosa due to mucosal barrier alterations
  3. causes- aspirin, toxins, alcohol, stress, CNS trauma or hypersecretion of gastric acid.
  4. The symptoms of acute gastritis range abdominal discomfort to massive, life-threatening hemorrhage and gastrical perforation
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11
Q 
chronic gastritis
 what is it characterized by
 leads to...
 type A
 type B
 hypersecretory vs environmental
A
  1. characterized by the absence of grossly visible mucosal erosions and by chronic inflammatory changes
  2. leads eventually to gastric mucosa atrophy and possibly carcinoma.
  3. The type A = autoimmune origin and is associated with pernicious anemia.
  4. Type B chronic gastritisis of nonimmune origin and is more common.
  5. hypersecretory- antral gastritis => duodenal ulcer or environmental -multifocal => gastric ulcer & carcinoma
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12
Q 
Acute peptic ulceration (stress ulcer)
 etiology
 where they start
 development of uclerations
 pathogenesis
A
  1. extension of acute erosive gastritis where the mucosal erosions penetrates the muscularis mucosa.
  2. They starts in the proximal part but multiple ulcers may involve entire stomach.
  3. appear within 24h after severe trauma, acute brain damage, severe medical illness, surgery, steroid therapy and aspirin abuse. 4. The pathogenesis is uncertain since acid concentration is not increased. They cause bleeding & DO NOT progress to chronic ulcers.
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13
Q 
chronic peptic ulcer
 what it affects
 results from
 duodenal ulcer
 gastric ulcer
A
  1. affects 5-10% of general (mid-adult) population.
  2. Resulting from acid-pepsin digestion of mucosa as solitary lesions occurring in duodenum or stomach.
  3. duodenal ulcer are increased in patients with a genetic predisposition (men, type 0 blood), who smoke and drink. They have acid secretion higher than in normal or patients with gastric ulcer
  4. gastric ulcer is more related to alteration of gastric mucosal resistance than to increased acid secretion and usually is extension of chronic gastritis.
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14
Q

hemorrhoids
def and location of internal vs. external
symptoms
predisposing factors (3)

A
  1. Persistently elevated venous pressure in hemorrhoidal plexus causes variceal dilatation of veins beneath rectal (internal hemorrhoids) and/or anal (external hemorrhoids) mucosa.
  2. When symptomatic, they produce pain, itching & rectal bleeding.
  3. Predisposing factors include chronic constipation, portal hypertension and pregnancy.
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15
Q 
acute appendicitis
 def 
 sciency def
 clinical signs
 complications
A
  1. intestinal inflammatory disease probably initiated by obstruction of mucus drainage which may lead to distension and bacterial infection.
  2. Neutrophil emigration from blood vessels is followed by fibrinopurulent exudation, suppurative necrosis of the mucosa resulting in gangrenous necrosis and predisposing to rupture.
  3. Clinically it is characterized by abdominal discomfort in the right lower quadrant, nausea, vomiting. 4. Complications are rupture, peritonitis, sepsis and death.
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16
Q

Ulcerative colitis
def and etiology
development of disease

A
  1. acute and chronic inflammatory disease of unknown etiology (possibility of an as yet unidentified infectious agent or immunologic mechanism) causing extensive ulcerations of the mucosal surface of the colon.
  2. begins as mucosal hemorrhages, abscesses and ulcerations in the rectum and spreads proximally and extend to the muscular layer. It is a recurrent disease manifested in young adulthood as abdominal pain, cramps & bloody diarrhea.
17
Q

hepatitis

A
  1. viral liver inflammatory disease by any viral agents
  2. A, B,C, or D
  3. acute or chronic
18
Q 
hep A
 what it is
 incubation period and symptoms
 how is it confirmed?
 progression? 
 vaccine?
A
  1. RNA virus liver infection acquired by ingestion of fecally contaminated food or water (associated with childhood and poor sanitary conditions).
  2. After incubation period (two to six weeks) patients develop nonspecific symptoms like fever, malaise and liver damage and jaundice
  3. confirmed by rise in serum aminotransferase activite
  4. Type A never progress to chronic hepatitis and infection provide lifelong immunity. Vaccine is available.
19
Q 
hep B
 disease
 how is it transmitted?
 acute
 fulminant
 chronic
A
  1. DNA virus acute and chronic liver infection which may be asymptomatic or exceedingly fulminant.
  2. virus is transmitted by blood products or contaminated needles
    and incubation period of up to six months hepatitis B can develop in:
  3. acute/ self limited: symptoms appear 2-3 months after exposure,complete recovery & lifelong immunity
  4. fulminant: massive liver necrosis, failure & death (in violent short time = fulminant def)
  5. chronic carrier state: patients do not develop antigens, infection persists and progress to chronic
20
Q

Hepatitis C

A

Hepatitis C is a RNA virus acute or chronic liver infection with clinical symptoms similar to that of hepatitis B. It is a result of transfusion of contaminated blood but, may be spread by the fecal-oral route. Recently developed screening test allowed testing of blood and incidence of hepatitis C begin to decline.

21
Q

hep D

A

is a RNA delta (defective) virus liver infection that requires help from coexisting hepatitis B virus infection with clinical course similar to hepatitis B.

22
Q 
cirrhosis
 characterized by...
 Laennecs cirrhosis
 physical changes to liver with Laennecs 
 symptoms of Laennecs
A
  1. characterized by necrosis, fibrosis & disruption of normal liver architecture.
  2. Laennec’s (alcoholic) cirrhosis is the common type in the U.S. (about 90% of the patients give a history of chronic alcoholism but only 10-15% of alcoholics develop cirrhosis) causing liver decreases in size with fine nodularity (micronodules).
  3. In advanced stages the liver develop fibrotic consistency and dark color.
  4. Cirrhosis may develop over a period of decades with symptoms of weight loss, nausea, vomiting, jaundice. Patients may develop ascites, esophageal varices, gastritis and death usually occurs from hepatic failure
23
Q 
postnecrotic (macronodular) cirrhosis 
 % of cirrhosis
 generally follows...
 how the liver looks 
 symptoms are a result of
 generally associated with...
A
  1. comprises between 10 and 30% of the total cases of cirrhosis
  2. generally follows a single episode of viral hepatitis or chronic hepatitis, or drug related hepatotoxicity which results in a marked degree of acute necrosis. 3. The liver is small with large, irregular regenerative nodules (macronodules) interspersed among scars of varied size and prominent bile stasis.
  3. When symptoms occur, they are usually the result of liver failure or portal hypertension.
  4. most frequently associated with liver carcinoma.
24
Q

Portal hypertension
why does it develop
what it is
what it leads to (2)

A
  1. most frequently seen as a complication of cirrhosis.
  2. Obstruction of the hepatic veins results in a backup of blood causing increased pressure in the portal vein which lead to:
    a) ascites: is the intraperitoneal accumulation of watery fluid chemically similar to plasma. Drainage of such fluid produces considerable loss of proteins and electrolytes.
    b) esophageal varices and hemorrhoids
25
Q

Cholelithiasis
def
3 primary constituents
%s and who they affect

A
  1. refers to accumulation of gallstones in gallbladder.
  2. three primary constituents: cholesterol (most common, with size from small up to 6 cm in diameter and egg-shell surface), calcium bilirubinate (less common, related to excessive production of bilirubin), calcium carbonate (rare).
  3. Mixed stones account for 80% of all biliary calculi. Gallstones are more seen in women, increase in incidence with age, and are related to obesity and high caloric diets.
26
Q

obesity

A

is an accumulation of body fat above a particular standard. If standard is 20% above the mean adiposity, then 20% of middle-aged man and 40% women are obese in US.

27
Q

Malnutrition
%
marasmus
kwashiorkor

A
  1. malnutrition = weight falls to 20% below normal
  2. marasmus- body weight falls 40% below norma. It is a result of loss of fat followed by catabolism of tissue proteins resulting in reduction of the skin thickness and muscle mass and decrease in serum proteins
  3. kwashiorkor- protein deprivation is greater than calorie reduction
28
Q

Hypopituitarism
what is it
how you get it
2 causes

A
  1. mean decrease secretion of adenohypophyseal hormones
  2. congenital, or may occur during the life with the effects related to deficit in one or a few hormones
    causes-
    a. hypothyroidism (depressed production of glucocorticoids by adrenal gland or secretion of the gonadotropic hormones and loss of sexual functions)
    b. Alterations in growth hormone production cause in hypo- production dwarfism or in hyperproduction giantism (prior to adolescence) & acromegaly
29
Q

alterations in posterior pituitary function in secretion of ADH
results in…
what happens to these people
what happens to 1/4 of the people who have this

A
  1. results in diabetes insipidus.
  2. The person with diabetes insipidus has a tendency to become dehydrated (due to inability to concentrate urine) and also to “wash out” an electrolytes from his body fluids (polyuria, thirst, polydipsia).
  3. In 1/4 of the cases it is associated with brain tumor that require surgical treatment, but if not it can be treated by insufflating a small amount of synthetic vasopressin.
30
Q 
Hyperthyroidism 
 a.k.a. 
 what is it
 manifestations (10)
 worst case scenario
A
  1. a.k.a. thyrotoxicosis, or Graves’ disease
  2. hypermetabolic state produced by increased thyroid hormones. 3. manifested by hyperkinesia, emotional lability, increased appetite but decreased weight, muscle weakness with fine tremors, heat intolerance, warm moist skin, sweating, tachycardia, cardiac arrhythmias, exophthalmus.
  3. Sudden release of excessive amounts of thyroid hormones (thyroid storm) is emergency condition that can progress to coma.
31
Q 
Hypoadrenalism
 a.k.a. 
 what is it a result of
 manifestations (8)
 what happens to normal blood glucose levels
A
  1. a.k.a. Addison’s disease
  2. results from failure of the adrenal cortex to produce adenocortical hormones due to atrophy or TB related distruction. 3. It is manifested by fatigue, anorexia, weight loss, nausea & vomiting. Hypotension, serum decrease in sodium, chloride and bicarbonate ions and increase in potassium are caused by aldosterone deficiency.
  3. Normal blood glucose levels and fat and protein mobilization are altered due to cortisol deficiency due to impaired gluconeogenesis.
32
Q 
Hyperadrenalism
 a.k.a. 
 associated with (7)
 what happens to normal bood glucose levels
 Conns disease
A
  1. a.k.a. - Cushing’s dis.
  2. is associated with abnormal amounts of cortisol.
  3. manifested by “moon faces”, “buffalo hump”, truncal obesity, menstrual disorders, susce- ptibility to infection, muscle weakness, osteoporosis.
  4. Increased blood glucose level is due to enhanced gluconeogenesis and if lasts for many months it may “burn out” insulin producion cells & cause “adrenal diabetes”.
  5. Conn’s dis.- (hyperaldosteronism) extra cell. fluid vol. is increased with hypokalemia.
33
Q

The renal diseases can be classified into different general categories (3)

A
  1. acute renal shutdown
  2. chronic renal insufficiency
  3. nephrotic syndrome
34
Q

acute glomerulonephritis
what does it do
what does it result from
bio and cell explanation

A
  1. acute glomerulonephritis- condition that interferes with kidney function and causes acute renal shutdown include
  2. results from an antigen-antibody (antibodies are formed usually 1-3 weeks following infections by streptococci
  3. reaction in which the glomeruli become inflamed which causes total or partial blockage of large number of glomeruli and those that are not blocked develop increased permeability of the glomerular membrane, allowing large amounts of protein and red blood cells to leak into GF.
  4. Acute form frequently becomes chronic.
35
Q

acute renal shut down
what causes it? (2)
and what causes those? (3)

A
  1. Acute damage to the tubules and necrosis
    The causes of tubular damage and necrosis are:
  2. poisons: (carbon tetrachloride and mercuric ions have specific nephrotoxic action)
  3. severe acute renal ischemia (is usually result from severe circulatory shock when heart fails to pump sufficient amounts of blood to the body)
  4. transfusion reaction (where hemolysis of large amounts of red blood cells releases hemoglobin (that precipitate in the nephron) and vasoconstrictor agent diminishing renal blood flow)
36
Q

chronic renal insufficency
main cause
what causes that? (5)

A
  1. decreased number of nephrons. The different causes of this include:
  2. chronic glomerulonephritis and pyelonephritis
  3. traumatic or congenital absence of a kidney
  4. congenital polycistic disease: when large cysts develop in the kidneys and destroy surrounding nephrons by compression
  5. urinary tract obstruction (caused by renal stones)
  6. arteriosclerosis: when small arteries supplying portions of the kidneys become blocked
37
Q

pyelonephritis
where it begins and ends
resultant of
meduallary function

A
  1. infectious and inflammatory process that usually begins in the renal pelvis and extends progressively into renal parenchyma.
  2. The infection can result from many types of bacteria, especially staphylococci and colon bacteria. which cause progressive destruction of the functional renal tissue, usually affecting more medulla of the kidney.
  3. Since one of the primary functions of the medulla is to provide the counter-current mechanism for concentration of the urine, patients have reasonably normal renal function with inability to concentrate urine.
38
Q

nephrotic syndrome
characterized by
this causes
diseases its associated with it (4)

A
  1. characterized by loss of large quantities of plasma proteins into the urine due to increased permeability of the glomerular membrane
  2. causing fall in colloid osmotic pressure and serious edema.
    diseases its associated with:
  3. chronic glomerulonephritis
  4. amyloidosis (deposition of an abnormal proteinoid substance - amyloid, in the walls of the blood vessels)
  5. syphilis
  6. systemic lupus erythematosus

CM test 2 (8 decks)

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