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)
A 36-year-old man has a history of chronic liver disease and a movement disorder. The photograph shows an abnormality in the cornea of the eye. Lab finding reported?
Decreased serum ceruloplasmin
Wilson’s disease - autosomal recessive disease
Ceruloplasmin is an enzyme that is synthesized in the liver. It contains 6 atoms of copper in its structure.
Ceruloplasmin is secreted into the plasma where it represents 90% to 95% of the total serum copper concentration. The remaining 5% to 10% of copper is free copper that is loosely bound to albumin.
Ceruloplasmin is eventually taken up and degraded by the liver. The copper that was bound to ceruloplasmin is excreted into the bile. The gene defect in Wilson’s disease affects a copper transport system that produces a dual defect—decreased incorporation of copper into ceruloplasmin in the liver and decreased excretion of copper into bile. Accumulation of copper in the liver increases the formation of free radicals causing damage to hepatocytes.
Most likely cause of this disorder?
Explain the pathogenesis that results in the appearance of this liver?
Biventricular heart failure
Mottled, cut surface of the liver. The dark areas represent congested central veins. These findings are indicative of centrilobular necrosis (“nutmeg liver”), which is most often caused by left-sided heart failure (LHF) and right-sided heart failure (RHF).
LHF decreases cardiac output causing hypoperfusion of the liver. This results in ischemic necrosis of hepatocytes located around the central vein. RHF causes a backup of systemic venous blood into the central veins and sinusoids, which produces congestion of central veins and sinusoids and necrosis of hepatocytes around the central vein.
Clinical findings include painful hepatomegaly with or without jaundice. Increased transaminases are caused by ischemic necrosis. Left untreated, it may progress to cardiac cirrhosis with fibrosis around the central veins.
