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Aa Flashcards

1
Q

Most common organ affected by TB

A

KIDNEY (sterile pyuria)

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2
Q

Pneumoconioses

A

Silicois - tb
Berrylium - caseatibg grabuloma, lung cancer

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3
Q

Difference between tension and spontaneous ptx

A

Tension shifts trachea bc air is trapped in the pleural space

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4
Q

Behcet traiad

A

Uveitis, aphthous ulcers, genial ulcers after viral infection.

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5
Q

Triple therapy for H. Pylori gastritis
Quad

A

Clarithromycin, amox, PPI

Ppi, metronidazole, bismuth, tetracycline

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6
Q

Carcinoid syndrome symptoms

A

Bronchospasm, diarrhea, flushing of skin

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7
Q

Complication of acute pancreatitis

A
  1. Pancreatic pseudocyst-formed by fibrous tissue surrounding liquefactive necrosis and pancreatic enzymes
    Presents as an abdominal mass with persistently elevated serum amylase Rupture is associated with release ofenzymes into the abdominal cavity and
    hemorrhage.
  2. Pancreatic abscess- often due to Ecoli
    Presents as an abdominal pain, fever with persistently elevated serum amylase

Enzymes can chew on coagulation factors and the alveolar-cap interface.
4. DICandARDS

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8
Q

Complication of biliary atresia

A

Duodenal obstruction

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9
Q

Complication of chronic pancreatitis

A

Characterized by herniation of gallbladder mucosa into the muscular wall
(Rokitansky-AscholT sinus.

Porcelain gallbladder is a late complication
1. Shrunken, hard gallbladder due to chronic inflammation, fibrosis, and dystrophic calcification

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10
Q

Gallstone ileus

A

If cholecystits happens, inflammation. Of the gallbladder wall, can cause the wall to rupture thereby creating a fistula between the gallbladder wall and duodenum. Stones can then go to small bowel

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11
Q

New onset cholecystitis in an elderly women

A

Gallbladder cancer

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12
Q

Mesothelioma complication

A

Recurrent pleural effusions

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13
Q

Symptoms of sarcoidosis

A

Other commonly involved tissues include the uvea (uveitis). skin feutancous nodules or erythema nodosum), and salivary and lacrimal glands (mimics Sjogren syndrome)salmost any tissue can be involved

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14
Q

Whipped disease symptoms

A

C. Other common sites ofinvolvement include synovium ofjoints (arthritis). valves. lymph nodes, and CNS.

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15
Q

Complications of IBD

A

Toxic megacolon and carcinoma (risk is based on extent a colonic involvement and duration of disease: generally not a concern until > 10 years of diseasel
Screening colonoscopy for dysplasia which can progress to carcinoma
Primary sclerosing cholangitis and PrANcA.
postivity

Chrons
Cobblestone mucosa creeping fat. atld strictures (‘string-sign’ on imaging. Stranding fat - fat
Malabsorption with nutritional deficiency;

calciam oxalate nephrolithiasis, fistula formation, carcinoma, if colonic disease is present

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16
Q

Divertulosis complication

A

Colovesicular fistula presents with air (or stool) in urine.

Fistula- occurs If inflammation of the wall
cal structurieeds to rupture therefore wall can be linked to
bladder

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17
Q

if HbsAg is positive and HbcIGM +

A

Acute infection

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18
Q

if HbsAg is positive and HbcIGg+

A

Chronic inf

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19
Q

if HbsAg is negative and Hbc Ab neg

A

Vaccinated

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20
Q

if HbsAg is negative and HbcAb (IGG) positive

A

Past infection

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21
Q

Symptomatic hepatitis but only HBcIgM positive

A

Window period

22
Q

HBsAg positive HbcAb (IgM)

A

Acute

23
Q

HBsAg neg HbeAb neg HBcIgM POs HbsAb neg

A

Window

24
Q

HBsAg neg HbeAg neg HBcIGg POs HBsAb positiv

A

Resolved

25
Q

HBsAg neg HbeAb neg HbcAb (IGG)

A

Chronic

26
Q

Cirrhosis

A

C. Clinical features

Portal hypertension leads to
1. Ascites (fluid in the peritoneal cavity)
Hyperspleenism- enlarged spleen eats platelets and rbc /Congestive splenomegaly/hvpersplenism
ili. Portosystemic shunts (esophageal varices, hemorrhoids, and capital Medusa
iv. Hepatorenal syndrome (rapidly developing renal failure secondary to
cirrhosis)

  1. Decreased detoxification results in
    i Mental status changes, asterixis, and eventual coma (due to serum
    ammonia); metabolic, hence reversible
    il.
    Gynecomastia, spider angiomata, and palmar erythema due to hyperestrinism iii. jaundice
  2. Decreased protein synthesis leads to i.
    Hypoalbuminemia with edema
    ii. Coagulopathy due to decreased synthesis ofclotting factors; degree of
    deficiency is followed by PT. Dec epixode reductase
27
Q

Difference between nonalcoholic and alcoholic liver disease

A

IV. ALCOHOL-RELATED LIVER DISEASE
A. Damage to hepatic parenchyma due to consumption ofalcohol

B. Fatty liver is the accumulation offat in hepatocytes (Fig. 11.9A)
1. Results in a heavy, greasy liver: resolves with abstinence (Fig. 11.9B)
C. Alcoholic hepatitis results from chemical injury to hepatocytes: generally seen with binge drinking
1. Acclaldehyde (metabolite of alcohol) mediates damage.
3. Presents with painful hepatomegaly and elevated liver enzymes (AST > ALT);
may result in death
D. Cirrhosis is a complication oflong-term, chronic alcohol-induced liver damage;

  1. NONALCOHOLIC FATTY LIVER DISEASE
    A. Fatty change, hepatitis, and/or cirrhosis that develop without exposure to alcohol other known insult)
    B. Associated with obesity
    C. Diagnosis ofexclusion; ALT > AST
28
Q

Hemochromatosis
Symptoms
Labs
Diagnostic testing
Treatment
Complication

A
  1. Priinary hemochromatosis is due to mutations In the HFE gene, usually C282Y (cysteine is replaced by tyrosine at amino acid 282). Secondary- transfusions

C. Presents in late adulthood
I. Classic triad is cirrhosis, secondary diabetes mellitus, and bronze skin; other. findings include cardiac arrhythmias and gonadal dysfunction (due to testicular atrophy).

Labs show ferritin, inc ; TIBC Dec serum iron inc and inc transferín saturation.
3. Liver biopsy reveals accumulation of brown pigment in hepatocytes
Prussian blue stain distinguishes iron (blue) from lipofuscin (Fig. H UB). i.

D. Increased risk of hepatocellular carcinoma Bc increase free radicals

E. Treatment is phlebotomy,

29
Q

Wilson’s
Symptoms
Complications
Treatment

A

V. WILSON DISEASE
A. Autosomal recessive defect (ATP7B gene) in ATP-mediated hepatovte copper transport
I. Results in lack ofcopper transport into bile and lack of copper incorporation into ceruloplasmin
B. Copper builds up in hepatocytes, leaks into serum, and deposits in tissues.
1. Copper-mediated production ofhydroxy! free radicals leads to tissue damage.

C. Presents in childhood with
1. Cirrhosis
•
2. Neurologic manifestations (behavioral changes, dementia, chorea similar to Huntington and Parkinsonian symptoms due to deposition ofcopper in basal ganglia)
3. Kayser-Fleisher rings in the corneal

D. Labs show inc urinary copper, Dec serum ceruloplasmin, and inc copper on liver biopsy.

E. Increased risk ofhepatocellular carcinoma Bc increase free radicals

F. Treatment is D-penicillamine (chelates copper).

30
Q

Difference between PBS AND PBC

A

VIII.PRIMARY BILIARY CIRRHOSIS
A. Autoimmune granulomatous destruction of intrahepatie bile ducts
1. Classically arises in women (average age is 40 years)
2.
Associated with other autoimmune discases
B. Etiology is unknown; antimitochondrial antibody is present.
C. Presents with features of obstructive jaundice
D. Cirrhosis is a late complication,

IX. PRIMARY SCLEROSING CHOLANGITIS
A. Inflammation and fibrosis ofintrahepatic and extrahepatic bile ducts
1. Periductal fibrosis with an onion-skin* discoloration
1. Periductal fibrosis with an onion-skin* apptarance (Fig. 11.12)
2. Uninvolved regions are dilated resulting in a “beaded” appearance on con imaging.
B.
Etiology is unknown, but associated with ulcerative colitis; p-ANCA is often p
C. Presents with obstructive jaundice; cirrhosis is a late complication.
D. Increased risk of cholangiocarcinoma

Obstructive jaundice
Dark urine (due To bilirubinuria) and pale stool

Hypercholesterolemia with xanthomas
Steatorchea with malabsorption of fat-soluble

Bile salts deposits
skin thereforePruiTis. Bile can’t get to the
therefore bile salts can’t help with fat absorption - malabsorption and Steatorrhea

31
Q

Causes of HCc
Complication

A

XII. HEPATOCELLULAR CARCINOMA
A. Malignant tumor ofhepatocytes
B. Risk factors include
1. Chronic hepatitis (e.g., HBV and HCV)
2. Cirrhosis (e.g., alcohol, nonalcoholic fatty liver disease, hemochromatosis,
Wilson disease, and AlAT deficiency)
3. Anatoxins derived from Aspergillus- (induce p53 mutations)

C. Increased risk for Budd-Chiari syndrome
1. Liver infarction secondary to hepatic vein obstruction
2. Presents with painful hepatomegaly and ascites
D. Tumors are often delected late because symptoms are masked by cirrhosis; poor prognosis
E. Serum tumor marker is alpha-fetoprotein.

32
Q

MCC in ADPKD

A

Berry aneurysm

33
Q

ADPKD

A

Berry aneurysms, liver cysTs, Mvp, HTN bc of increases renin, hematuria

34
Q

Difference between Acute renal failure

A

II. PRERENAL AZOTEMIA
A. Due to decreased blood flow to kidneys (e.g., cardiac failure); common cause of ARf

B. Decreased blood How results in decreases GFR, azotemia, and oliguria.
C. Reabsorption offluid and BUN ensues (scrum BUN: Cr ratio > 15): tubular function remains intact (fractional excretion ofsodium
[FENa] < 1% and urine osmolality > 500 mOsm/kg).

IV ACUTE TUBULAR NECROSIS
A. Injury and necrosis oftubular epithelial cells (Fig, 12,5); most common cause of acute renal failure (intrarenal azotemia)
B. Necrotic cells plug tubules; Dysfunctional tubular epithelium results in decreased reabsorption of BUN (serum
BUN:Cr ratio < 15), decreased reabsorption ofsodium (FENa > 2%), and inability to concentrate urine (urine osm < 500 mOsm/kg).
D. Etiology may be ischemic or nephrotoxic,
Ischemia - Decreased blood supply rosults in And this decreased blood flow persists . Often preceded by prerenal
il. Proximal tubule and medullary segment ofthe thick ascending limb are
particularly susceptible to ischemic damage.
2. Nephrotoxic -Toxic agents result in necrosis oftubules.
i. Proximal tubule is particularly susceptible.
il. Causes include aminoglycosides (most common), heavy metals (e.g., lead), myoglobinuria (e.g., from crush injury to muscle), ethylene glycol (associated with oxalate crystals in urine), radiocontrast dye, and urate (c.g., tumor lysis syndrome).
ill. Hydration and allopurinol are used prior to initiation ofchemotherapy to
decrease risk of urate-induced AT.

III. POSTRENAL AZOTEMIA
to obstruction of urinary tract downstream from the kidney (e.g., ureters). During early stage of obstruction, increased tubular pressure “forces” BUN into the
therefore blood (serum BUN;Cr ratio > 15); tubular function remains intact (FENa < 1% and can concentrate urine therefore tubular function is
urine osm > 500 mOsm/kg) perserved
D. With long-standing obstruction, tubular damage ensues, resulting in decreased reabsorption of BUN (serum BUN:Cr ratio < 15), decreased reabsorption ofsodium (FF^Na > 2%), and inability to concentrate urine (urine osm < 500 mOsm/kg).

35
Q

Ain

A

V. ACUTE INTERSTITIAL NEPHRITIS
A. Drug-induced hypersensitivity involving the interstitium and tubules (Fig. 12.6);
results in acute renal failure (intrarenal azotemia)
B. Causes include ((NSAIDs, penicillin, and diuretics)
C. Presents as oliguria, fever, and rash days to weeks after starting a drug; cosinophils may be seen in urine.
D. Resolves with cessation of drug
E. May progress to renal papillary necrosis

VI, RENAL PAPILLARY NECROSIS
A. Necrosis of renal papillae
§. Presents with gross hematuria and flank pain
C. Causes include
1. Chronic analgesic abuse (e.g.. long-term phenacetin or aspirin use)
2. Diabetes mellitus
3. Sickle cell trait or disease
4. Severe acute pyelonephritis

36
Q

Mc affected organ in systemic amyloidosis

A

Renal (nephrotic )

37
Q

I’m SLE, MCCOD

A

Renal failure (from diffuse proliferative

38
Q

Causes of nephrotoxic ATn

A

D. Etiology may be ischemic or nephrotoxic, !.
Ischemia- Decreased blood supply results in necrosis of tubules.
And this decreased blood flow persists resulting in
i.
Often preceded by prerenal azotemia
Atn
ii. Proximal tubule and medullary segment ofthe thick ascending limb are
particularly susceptible to ischemic damage.
2. Nephrotoxic-Toxic agents result in necrosis oftubules.
i. Proximal tubule is particularly susceptible.
ii. Causes include aminoglycosides (most common), heavy metals (e.g., lead), myoglobinuria (e.g., from crush injury to muscle), ethylene glycol (associated with oxalate crystals in urine), radiocontrast dye, and urate (e.g., tumor lysis syndrome).
iii. Hydration and allopurinol are used prior to initiation of chemotherapy to
decrease risk of urate-induced ATN.

39
Q

Renal papillary necrosis

Sxs
What causes it

A

VI, RENAL PAPILLARY NECROSIS
A. Necrosis of renal papillae
8. Presents with gross hematuria and flank pain
C. Causes include
1. Chronic analgesic abuse (e.g., long-term phenacetin or aspirin use)
2. Diabetes mellitus
3. Sickle cell trait or disease
4. Severe acute pyelonephritis

40
Q

Minimal change disease

Diagnostic
Treatment
Complication

A

C. Normal glomeruli on H&E stain (lipid maybe seen in proximal tubule cells.
D. EfTacement of foot processes on electron microscopy (F.M, Fig. 12.7B)
E. No immune complex deposits; negative immunofluorescence (IF)
F. Selective proteinuria (loss of albumin, but not immunoglobulin)
G. F.xcellent response to steroids (damage is mediated by cytokines from T cells)- if doesn’t resolve can lead to FSGS

Complication of : Usually idiopathic; may be associated with Hodgkin lymphoma
I.
Cytokines damages the podocyte and Hodgkin is caused by cytokines
-

41
Q

Sxs of nephrotic

A
  1. BASIC PRINCIPLES
    A. Glomerular disorders characterized by proteinuria (> 3.5 g/day) resulting in
  2. Hypoalbuminemia pitting edema
  3. Hypogammaglobulinemia–increased risk ofinfection
  4. Hypercoagulable state- -due to loss of antithrombin III
    Hrperlipidemia and hypercholesterolemia-may result in fatty casts in urine
42
Q

FSGS
- diagnostic testing
- treatment
-associated with what conditions

A

III. FOCAL SEGMENTAL GLOMERULOSCLEROSIS (FSGS)
A. Most common cause of nephrotic syndrome in Hispanics and African Americans
Sclerosis - pink deposits
Usually idiopathic; maybe associated with HIV, heroin use, and sickle cell disease
C. Focal (some glomeruli) and segmental (involving only part of the glomerulus)
sclerosis on H&E stain (Fig. 12.8)
D. Fffacement of foot processes on EM
E. No immune complex deposits; negative IF
Foor response to steroids, progresses to chronic renal failure

43
Q

Membranous
-associated with what conditions
- diagnostic testing
- treatment
- antibody

A

Thick not thin filtration barrier b of immune complex deposition
Epithelial lays down additional basement / membrane creatin‹
IV. MEMBRANOUS NEPHROPATHY
dome over deposits. Spikes in
A. Most common cause of nephrotic syndrome in Caucasian adults
between dome
B. Usually idiopathic; may be associated with hepatitis B or C, solid tumors, SLE, or drugs (e.g.. NSAIDs and penicillamine)

IV. MEMBRANOUS NEPHROPATHY
A.
Most common cause of nephrotic syndrome in Caucasian adult
B.
Usually idiopathic; may be associated with hepatitis B or C, solid tumors, drugs (e.g. NSAIDs and penicillamine)

Thick glomerular basement membrane on H&E (Fig. 12.9A)

Due to immune complex deposition (granular IE , subepithelial deposits ‘spike and dome’ appearance on EM (Fig. 12.9C)
E. Poor response to steroids: progresses to chronic renal failure

Antibodies against Pla2R (phospholipase)

44
Q

Membrane proliferative glomerulonephritis

  • associated with what conditions
  • diagnostic testing
  • treatment
A

V. MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS
A. Thick glomerular basement membrane on H&E, often with ‘tram-track’ appearance
B. Due to immune complex deposition (granular IF
C. Divided into two types based on location of deposits

  1. Type I-_ subendothelial (Fig. 12.10); associated with HBV and HCV- tram tracks
    2, Type II (dense deposit disease) intra membranous; associated with C3 nephritic factor (autoantibody that stabilizes C3 convertase, leading to overactivation of complement, inflammation, and low levels of circulating C3)
    Under normal conditions C3
    D. Poor response to steroids; progresses to chronic renal failure
45
Q

Dm
- nephrotic / nephritic
- creates what?

A

Glucose in basement membrane causes leakage of it releasing protein which narrows the lumen. Hyaline arterial in the efferent arteriole therefore inc pressure in glomerulus leading to sclerosis of glom mesangial progresses to nephrotic j and hyper filtration (microalbuminuria -ACEi prevents this bc blocks ang 2

B. Glomerular efferent arteriole is more affected than the afferent arteriole, leading to high glomerular filtration pressure.
L. Hyperfiltration Injury leads to microalbuminuria,
C. Eventually progresses to nephrotic syndrome
1. Characterized by sclerosis of the mesangium with formation of Kimmelstiel-Wilson nodules (Fig. 12,111
D. ACE inhibitors slow progression of hyper hitration-induced damage

46
Q

most commonly involved organ in systemic amyloidosis.

A

A. Kidney is the most commonly involved organ in systemic amyloidosis.

Amyloid deposits in the mesangium, resulting in nephrotic syndrome,
C. Characterized by apple-green birefringence under polarized light after staining with Congo red

47
Q

Nephritic

A

I. BASIC PRINCIPLES
A. Glomerular disorders characterized by glomerular inflammation and bleeding
1. Limited proteinuria (< 3.5 g/day)
2. Oliguria and azotemia
•
3. Salt retention With periorbital edema and hypertension SHa0 velenhon
4. RBC casts and dysmorphic RBCs in urine
When glomerular bleeds, d casts are formed in the shape of the tubular.
B. Biopsy reveals hypercellular, inflamed glomeruli (Fig. 12.12).
neu

48
Q

PSGn
- diagnostic testing
- treatment

A

I. POSTSTREPTOCOCCAL GLOMERULONEPHRITIS (PSGN)
A. Nephritic syndrome that arises alter group A |3-he mo lytic streptococcal infection Of the skin (impetigo) or pharynx
1. Occurs with nephritogenic strains (which carry the M protein virulence factor)
2. May occur after infection with nonstreptococal organisms as well
B. Presents 2-3 weeks after infection as hematuria (cola-colored urine), oliguria, hypertension, and periorbital edema
1. Usually seen in children, but may occur in adults
C. Hypercellular, inflamed glomeruli on H&E
D. Mediated by immune complex deposition (granular IF)- immune complex deposition activates C5a which attracts neutrophils

; subepithelial ‘humps’ on
EM )
Deposits start subendothelial, deposits can disappear therefore it resolves
E. Treatment is supportive
1. Children rarely (1%) progress to renal failure.
2. Some adults (25%) develop rapidly progressive glomerulonephritis (RPGN).

49
Q

RPGN
- testing

A

Linear (anti basement membrane of lung and kidney -Goodpasture syndrome)
Antibody attacks the basement of lung

Granular (immune complex deposition)
-PSGN OR RPGN
Diffuse proliterative glomerulomephritis is duc to diffusc antigen - a lit ib ody complex deposition, usually sub-endothehal, most common type ofrenal disease in SLE

Negative II (pauci-immunc)
Do anca

B. Characterized by crescents in Bowman space (of glomeruli) on H&E stain; crescents are comprised of fibrin and macrophages (Fig. 12 14).

50
Q

IGA nephropathy

  • diagnostic
A

IV. IgA NEPHROPATHY (BERGER DISEASE)
A, IgA immune complex deposition in mesangium ofglomeruli; most common
nephropathy worldwide
B, Presents during childhood as episodic gross or microscopic hemaluria with RBC
easts, usually following mucosal infections (e.g., gastroenteritis)
1. IgA production is increased during infection.
C. IgA immune complex deposition in the mesangium is seen on IF (Fig. 12.16).
D. May slowly progress to renal failure

<1 week after URI

51
Q

Al port

A

V, ALPORT SYNDROME
A. Inherited defect in type IV collagen; most commonly X-linked (Col4A5 mutation
B. Results in thinning and splitting of the glomerular basement membrane (basket weave pattern -EM
C. Presents as isolated hematuria, sensory hearing loss, and ocular disturbances- damaged basement membrane in ears, eyes, kidney in family

52
Q

Features of chronic renal failure

A

I. BASIC PRINCIPLES
A. End-stage kidney failure
1. May result from glomerular, tubular, inflammatory, or vascular insults
2. Most common causes are diabetes mellitus, hypertension, and glomerular discasc,
B. Clinical Features
1. Uremia–Increased nitrogenous waste products in blood (azotemia) result in nausca, anorexia, pericarditis, platelet dysfunction, encephalopathy with asterixis, and deposition of urea crystals in skin,
2. Salt and water retention with resultant hypertension
3. Hyperkalemia with metabolic acidosis
Can’t get rid of
4. Anemia due to decreased erythropoietin production agriensi peritubular
interstitial cells
5. Hypocalcemia due to decreased I-alpha-hydroxylation ofvitamin D by proximal renal tubule cells and hyperphosphatemia
6, Renal osteodystrophy due to secondary hyperparathyroidism, osteomalacia, and osteoporosis
C. Treatment involves dialysis or renal transplant.
1. Cysts often develop within shrunken end-stage kidneys during dialysis,
increasing risk for renal cell carcinoma.
cysts in already shrunken kidney

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