Goljan RR Q-Bank Flashcards
Present in patient with viral hepatitis
- Apoptotic bodies (deeply eosinophilic bodies with or without a pyknotic nucleus)
- lymphocyte-predominant infiltrate in the portal triads
Periodic acid–Schiff-positive granules in hepatocytes
α1-antitrypsin (AAT) deficiency, an autosomal dominant disorder
Which of the following histologic findings is most likely present in the liver in a child with Reye’s syndrome?
Microvesicular fatty change
usually develops in children < 4 years of age who receive aspirin (acetylsalicylic acid) to reduce fever associated with a viral respiratory infection or chickenpox.
- Salicylates damage the mitochondria in the liver, which disrupts the urea cycle and β-oxidation of fatty acids.
- Disruption of the urea cycle causes an increase in serum ammonia, which produces an encephalopathy characterized by cerebral edema, papilledema, and coma.
- Disruption of β-oxidation of fatty acids in the liver causes microvesicular fatty change, in which small globules of fat in the cytoplasm surround a centrally located nucleus
A 25-year-old woman is a type 1 diabetic in ketoacidosis. Which of the following best explains the mechanism for her hyperlipoproteinemia?
Decreased activation and release of capillary lipoprotein lipase (CPL)
Lack of insulin in diabetic ketoacidosis decreases activation and release of CPL, which is required to hydrolyze chylomicrons from the diet into a chylomicron remnant and VLDL into intermediate density lipoprotein (IDL) and LDL.
type V hyperlipoproteinemia
Achilles’ tendon xanthomas are pathognomonic for this disease
Polycythemia vera may lead to this liver disease.
Hepatic vein thrombosis
posthepatic obstruction of blood flow. Blood builds up behind the obstructed hepatic vein and produces congestion of the central veins in the liver (painful hepatomegaly) with concomitant necrosis of the zone III hepatocytes (markedly increased serum transaminases). The increased pressure extends into the portal vein (portal vein hypertension) leading to ascites and splenomegaly.
- high mortality with approximately 75% mortality in the first year
A 57-year-old man presents with a 6-month history of severe constant pain in the splenic flexure area shortly after eating. He states that the pain is so intense that he is afraid of eating and has lost approximately 23 kg (50 pounds). Recently, he has noticed blood in his stools.
Ischemic colitis involves the splenic flexure of the large bowel, which is a watershed area of two overlapping blood supplies—superior mesenteric artery and inferior mesenteric artery.
- The pain in the splenic flexure after eating is classic mesenteric angina due to decreased blood flow to the splenic flexure.
- barium enema shows “thumb-printing” of the colonic mucosa due to edema of the mucosa from infarction.
Presentation of Angiodysplasia
Occurs in the cecum and presents with a sudden massive loss of blood (hematochezia) without pain. It is due to rupture of telangiectatic vessels in the cecum.
- large volumes of blood per rectum (hematochezia) that are capable of producing dizziness due to hypotension or hypovolemic shock
- Angiodysplasia refers to the presence of dilated vascular channels in the submucosa of the cecum, which often rupture and produce massive lower gastrointestinal bleeding.
Most specific test fo acute pancreatitis
Serum lipase is a more specific test for acute pancreatitis than serum amylase, which may be normal in the serum after 2 to 4 days.
Lipase initially increases in 3 to 6 hours; peaks in 12 to 30 hours, and returns to normal in 7 to 14 days.
Level of immunoreactive trypsin in acute v chronic pancreatitis.
Serum immunoreactive trypsin is increased (not decreased) in 95% to 100% of cases of acute pancreatitis. It is decreased in chronic pancreatitis.
Physical findings of
- abdominal distention,
- tympany to percussion,
- absences of rebound tenderness, and
- high-pitched tinkling sounds on auscultation are classic findings of:
Bowel obstruction
Patient’s history of colicky pain (pain followed by a pain-free interval) is characteristic of a small bowel obstruction
Adhesions from previous surgery are the most common cause of bowel obstruction
Presentation of large bowel infarction
Most common cause of small bowel infarction?
bloody diarrhea and localized, noncolicky abdominal pain.
Atherosclerosis or embolism to the superior mesenteric artery is the most common causes of a large bowel infarction
Serum Na/K+ and Cl/HCO3 levels in a patient with cholera?
serum Na+ 138, (135−147 mEq/L) Loss of isotonic fluid does NOT alter serum Na+ concentration.
serum K+ 2.2, (3.5−5.0 mEq/L) Diarrheal fluid is rich in K+ and HCO3-; Results in hypokalemia
serum Cl− 114, (95−105 mEq/L) Increased because it replaces the bicarb anions that are lost in the diarrheal fluid to maintain elcroneutrality
serum HCO3− 14 (22−28 mEq/L) Diarrheal fluid is rich in K+ and HCO3-; Results in metabolic acidosis
Serum electrolytes in Addison’s disease?
**mineralocorticoid deficiency **
- Hyperkalemia (Peaked T waves)
- Hyponatremia
- Metabolic acidosis - retention of H+
inhibition of Na+ reabsorption and K+ secretion by the aldosterone-dependent Na+ and K+ channels located in the distal tubule and collecting ducts causing a hypertonic loss of Na+ in the urine (hyponatremia) and retention of K+ (hyperkalemia with peaked T waves)
serum Na+ 128,
serum K+ 5.9,
serum Cl− 96,
serum HCO3− 20) - Due to dysfunction of the aldosterone-dependent H+/K+ ATPase pump in the collecting tubules, there is retention of H+ ions and a subsequent lack of synthesis of HCO3−, which produces metabolic acidosis
Serum electrolytes in Primary aldosteronism
Exactly why does this acid-base status exist?
- serum Na+ 152,
- serum K+ 2.8,
- serum Cl− 110,
- serum HCO3− 33
mineralocorticoid excess (e.g., primary aldosteronism; 11-hydroxylase deficiency
- hypernatremia
- hypokalemia
- metabolic alkalosis (Na exchanges with H+, for every H+ lost in the urine, there is a corresponding HCO3- entering the blood)
Clinical findings:
- weight loss,
- change in consistency of stools
- constipation
- blood mixed in with stools
highly predictive of colorectal cancer
complicated by iron deficiency anemia (microcytic anemia and decreased serum ferritin)
Type of necrosis occuring in Acute pancreatitis?
Enzymatic fat necrosis
Lipase converts triglyceride in adipose cells to fatty acids, which combine with calcium salts to form soap (called saponification). The pancreas in the photograph shows dark areas of hemorrhage and focal areas of pale fat necrosis in the peripancreatic fat (upper left).
Which populations is lactase deficiency common?
Lactase deficiency is a common genetic defect in Native Americans, Asians, and blacks.
Best explains the pathogenesis of the liver disease seen in alcoholics?
Increased synthesis of glycerol 3-phosphate (G3-P)
Alcohol metabolism results in:
- increased production of nicotinamide adenine dinucleotide plus hydrogen (NADH) in alcohol metabolism.
- An increase in NADH increases conversion of dihydroxyacetone phosphate to G3-P, which is the primary substrate for the synthesis of triglyceride in the liver.
- excess triglyceride as clear spaces in the cytosol of hepatocytes
- decreases β-oxidation and increases the concentration of fatty acids
- Fatty liver is a characteristic
Discrete raised white patches (leukoplakia) on both sides of the tongue. Greatest risk factor for developing this type of lesion?
Cigarette smoking is the greatest risk factor for squamous cell cancer in the mouth and oropharynx
Serum and urine laboratory test abnormalities would you expect to see in Gilbert’s disease?
% CB Urine Bilirubin Urine UBG AST ALT ALP GGT
** <20 ** ALL of the rest NORMAL
Gilbert’s disease, which is an autosomal dominant disease characterized by decreased uptake and conjugation of bilirubin particularly exacerbated by the fasting state
- Baseline unconjugated bilirubin (UCB) levels are increased to over twice normal in the fasting state leading to visible evidence of jaundice (CB < 20%)
- second overall most common cause of jaundice in the United States
Laboratory findings indicative of obstruction of bile flow.
Quick test that would indicate signs of obstruction?
- increased serum bilirubin, most of which is conjugated (>50% of the total)
- greater increase in alkaline phosphatase and GGT than in ALT and AST
- urine dipstick would show an absence of urobilinogen and increased bilirubin, signs of obstruction.
A 28-year-old woman who has been taking oral contraceptives for the past 10 years suddenly develops abdominal pain and dizziness while exercising. In the emergency department, physical examination shows that the patient has hypotension and a distended abdomen. A pregnancy test is negative. Surgical exploration shows blood in the abdominal cavity. Which of the following is the most likely cause of the intra-abdominal hemorrhage?
Ruptured liver cell (hepatic) adenoma
Liver cell (hepatic) adenomas are a complication of oral contraceptive use. These benign tumors arise from hepatocytes and have a tendency to rupture and cause intraperitoneal hemorrhage.
Although cavernous hemangiomas are the most common benign tumors of the liver and can rupture, they do not have an association with previous use of oral contraceptives.
Why does serum sodium concentration not change when volume depleted?
Loss of isotonic fluid does not alter the serum Na+ concentration (↔serum Na+ = ↓TBNa+/↓TBW); however, the decrease in TBNa+ causes signs of volume depletion (dry mucous membranes, poor skin turgor, hypotension).
