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AB&SS2 > C4: Metabolic Diseases > Flashcards

C4: Metabolic Diseases Flashcards

1
Q

hepatocellular disease is due to dysfunction of which cells in the liver

A

hepatocytes

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2
Q

describe fatty infiltration

is it acquired

A

accumulation of triglycerides w/in hepatocytes that can be diffuse or focal… its a precursor to chronic disease

yes, and reversible by lifestyle

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3
Q

2 most common causes of fatty infiltration

A

alcohol abuse and obesity

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4
Q

what 4 specific things do we evaluate w/ fatty infiltration

A

echogenicity changes
echotexture changes
attenuation characteristics
ability to visualize vessels/pausity

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5
Q

what technical parameters are important to optimize when assessing fatty infiltration

A

gain, TGC and focus

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6
Q

another term for fatty infiltration

A

steatosis

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7
Q

describe the US appearance of mild (grade 1) fatty infiltration

A

slight increase in echogenicity

diaphragm and vessels well seen

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8
Q

describe the US appearance of moderate (grade 2) fatty infiltration

A

increased liver echogenicity

diaphragm and vessels not sharply defined

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9
Q

describe the US appearance of severe (grade 3) fatty infiltration

A

echogenicity markedly increased

very hard to define diaphragm and vessel walls

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10
Q

describe focal fatty changes

2 types

A
  • focal areas of altered echogenicity that commonly occur in the periportal area of the medial left lobe
  • can change rapidly in short periods of time

focal fatty infiltration
focal fatty sparing

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11
Q

how do the boundaries of focal fatty changes appear

does FFC show the mass effect

A

map like, not like a mass

no

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12
Q

describe focal fatty infiltration

A

focal areas of increased echogenicity w/ mostly normal liver tissue

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13
Q

describe focal fatty sparing

A

mostly fatty liver tissue w/ focal hypoechoic areas of norm liver tissue

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14
Q

potential lab value changes w/ fatty infiltration

A

ALT, AST, GGT

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15
Q

describe cirrhosis

A

a diffuse and progressive process that destroys liver cells and results in liver fibrosis w/ nodular changes

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16
Q

most common cause of cirrhosis

other causes

A

alcohol abuse

multiple causes chronic viral hepatitis, primary sclerosing cholangitis

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17
Q

chain of events w/ cirrhosis

is it reversible

A

cell death, fibrosis, regeneration

no, but the progression can be slowed

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18
Q

2 types of nodular changes w/ cirrhosis

A

micro nodular - due to alcohol consumption

macro nodular - due to chronic viral hepatitis

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19
Q

describe acute and chronic cirrhosis

A

acute - same appearance of severe fatty infiltration (enlarged liver, coarse textural changes)

chronic - small liver, course texture, nodular surface and paucity of vessels

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20
Q

what can cirrhosis lead to

A

portal hypertension and then end stage liver failure

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21
Q

what lab values might be increase w/ cirrhosis

decrease

A

AST, ALT, LDH, ALK phos, GGT
conjugated bilirubin

albumin

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22
Q

which other organ can be affected by cirrhosis

why

A

spleen

portal hypertension

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23
Q

classic clinical presentation of cirrhosis

A

hepatomegaly, jaundice and ascites

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24
Q

describe glycogen storage disease

A

an autosomal recessive disorder that causes an enzyme deficiency which leads to excessive glycogen deposits in the liver

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25
Q

another name for GSD

when does GSD start

A

von gierke’s disease

neonatally

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26
Q

GSD is associated w/ which conditions

A

benign adenomas and HCC

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27
Q

does a liver transplant help w/ GSD

how is GSD managed and controlled

A

no, enzyme deficiency still present

diet

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28
Q

US appearance of GSD

A

presents as diffuse fatty infiltration w/ adenomas that have variable echogenicity (often they appear hypo due to fatty liver)

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29
Q

define ascites

A

accumulation of serous fluid in a peritoneal cavity

can be transudate or exudate fluid

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30
Q

what is transudate fluid

A

fluid that contains little protein or cells and suggests a non-inflammatory process (cirrhosis or CHF)

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31
Q

what causes ascites w/ cirrhosis

A

hypoalbuminemia and increased pressure in the liver causing fluid to leak out of the hepatocytes

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32
Q

what disease process of the heart can cause ascites

A

CHF

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33
Q

what is exudate fluid

A

fluid w/ high protein content
….can contain blood, pus, chylous

suggests an inflammatory or malignant cause

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34
Q

define chylous

A

milky fluid w/ high fat content, usually from lymphatic system

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35
Q

US appearance of exudate ascites

A

fluid w/ internal echos and loculations

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36
Q

define free fluid vs loculated

A

free: conforms to surroundings and changes w/ patient position
loculated: walled off, no changes w/ position, will show mass effect

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37
Q

3 most dependent spaces in the peritoneal cavity

A

morrisons pouch
pouch of douglas
paracolic gutters

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38
Q

describe biliary sluge

other names for it

A

a mixture of particulate matter and bile

biliary sand and microlithiasis

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39
Q

most likely cause of biliary sluge

other causes

A

bile stasis

prolonged fasting
fast weight lost
IV nutrition (TPN - total parenteral nutrition)
extrahepatic biliary obstruction
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40
Q

progression of biliary stasis

A

asymp. , biliary colic and inflammation of GB and panc`

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41
Q

US appearance of biliary sluge

A

non shadowing, homogenous low level echos that layer in the dependent part of the GB (fluid-fluid levels)

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42
Q

describe tumefactive sludge/sludge balls

how can you tell the difference b/w them and polypoid tumors

A

sluge that mimics polypoid tumors

look at vascularity, mobility and GB wall thickness

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43
Q

most reliable way to tell the difference b/w polypoid tumors and tumefactive sludge/sludge balls

A

mobility (sludge is mobile, polyps don’t)

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44
Q

describe hepatization

A

when sludge has the same echogenicity as the liver

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45
Q

what is pseudosludge

A

an imaging artifact caused by gains, slice thickness or side lobe artifacts

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46
Q

one way to tell pseudosludge from true sludge

A

pseudosludge is usually seen in the fundus and is independent or gravity

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47
Q

what is empyema

A

pus is the bile

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48
Q

what is hemobila

common causes

A

blood in the bile often due to liver biopsy or percutaneous biliary procedures

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49
Q

describe milk of calcium

US appearance

A

GB becomes filled w/ semi solid substance (calcium carbonate), different than biliary sludge

highly echogenic w/ posterior shadowing that changes w/ patient position and forms a calcium/bile fluid level

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50
Q

most common disease of the GB

A

cholelithiasis

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51
Q

factors effecting GB stone formation/cholelithiasis

A

abnorm bile composition
stasis of bile
infection

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52
Q

most common composition of cholelithiasis

others

A

cholesterol

bilirubin
calcium

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53
Q

risk factors for cholelithiasis

A

5 Fs

female
fat
fourty
fertile
Fam Hx
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54
Q

clinical presentation of cholelithiasis

A

asymptomatic (common)
RUQ pain that radiates to the back
nausea and vomitting
belching

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55
Q

US appearance of cholelithiasis

stones smaller than what size may not shadow

A

echogenic focus w/ posterior shadowing
will be mobile and may float in bile

< 5mm

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56
Q

GB stones are commonly mistaken for which other structures

A

duodenal gas (most common)

valves of heister
fat in porta hepatis

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57
Q

how to tell b/w GB stone and duodenal gas

A

duodenal gas will parastalisis and you’ll see a direly shadow vs clean one w/ the stone

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58
Q

WES sign

A

an US sign seen when the GB is compacted w/ multiple stones or one large stone - W: wall E: echo S: shadow

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59
Q

altered lab values w/ GB stones

A

AST, ALT, ALP, bilirubin

60
Q

complications of GB stones

A
  • biliary colic - stone temporarily lodged in the GB neck causing severe pain
  • obstruction of cystic duct or CBD
  • bacterial infection
  • cholecystitis
  • ascending cholangitis - spreading of infection from GB to the rest of the biliary tree
61
Q

most common complication of GB stones

A

biliary colic

62
Q

what causes ducts to dilate

A

obstruction
loss of duct wall elasticity
dysfunction of ampulla of vater

63
Q

what should we look for on US w/ biliary tree obstruction

A

check for dilation of ducts or GB, if they’re dilated, @ what level and determine the cause

64
Q

clinical presentation of biliary obstruction

when are they see?

A

painless or painful jaundice

painless: w/ neoplastic conditions (check panc head) and choledocal cysts
painful: w/ acute obstruction and/or infection

65
Q

signs and symptoms of biliary obstruction

A

jaundice
clay coloured stool
abnormal LFTs
pain, nausea

66
Q

what is choledocholiathiasis

A

stones in the biliary tree, can be extra or intrahepatic

67
Q

primary and secondary causes of choledocholiathiasis

which is most common

A

primary: stones form in the ducts
secondary: stones pass from GB to ducts

secondary

68
Q

causes of primary choledocholiathiasis

A

inflammation
infection
carolis
surgery

69
Q

most common location for stones in the biliary tree

why can it be hard to visualize

A

distal CBD at the ampulla of vater

bowel gas…. look for hyper foci w/ posterior shadowing

70
Q

how can you improve visualization when looking for a stone @ the distal CBD

A

change patient position
compress bowel
change windows

71
Q

false + for stone in the distal CBD

A

surgical clips
air
edge artifact

72
Q

altered lab values w/ choledocholiathiasis

A

ALP, AST, ALT

bilirubin

73
Q

treatment for choledocholiathiasis

A

ERCP spincterotomy (enlarge the sphincter for stone to pass)
ERCP extraction
stenting

74
Q

what does ERCP stand for

A

endoscopic retrograde cholangiopancreatography

75
Q

define urolithiasis

A

stones in the urinary sys

76
Q

describe nephrolithiasis

most common in which gender

A
  • stones in the renal collection system
  • very common and unknown etiology
  • incidence increases with age

male, caucasian

77
Q

risk factors for nephrolithiasis

A

hereditary
limited water intake
animal protein
urinary stasis

78
Q

natural points of narrowing in the ureters

A

UPJ
iliac vessels
UVJ - narrowest part, 80% of stones get stuck here

79
Q

stones under what size can be passed

A

< 5mm (80% this size are passed)

80
Q

clinical presentation of nephrolithiasis

A

asymp
hematuria
flank pain

81
Q

what to look for w/ nephrolithiasis

A

number of stones
size
location
complications (look for hydro and jets)

82
Q

easy way to identify small stones

A

use colour and look for twinkling artifact

83
Q

what are staghorn calculi

A

calcifications filling the collecting system

84
Q

define nephrocalcinosis

A

calcifications in the renal parenchyma

85
Q

3 other DI modalities the can detect urolithiasis

A

Xray, tomography and CT

86
Q

cause of bladder calculi

what should you check for

A 
stone migrates from kidney
urinary stasis (neurogenic bladder or BPH)

mobility of the stone

87
Q

clinical presentation of bladder calculi

A

asymp
OR
hematuria
pain

88
Q

what do you need to check for if you suspect a stone in the ureter

A

jets and hydro to see if its obstructive or not

89
Q

describe hydronephrosis

what can it lead to

A

dilated renal collecting sys due to obstructive or non-obstructive causes

can lead to renal atropy

90
Q

obstructive causes of hydro

non-obstructive causes of hydro

A

O: can be intrinsic (stone, mass) or extrinsic (mass) obstruction

N-O: reflux, infection, polyuria

91
Q

what is polyuria

A

too much urine production

92
Q

which type of hydro can we diagnose on US

A

obstructive

93
Q

classifications of hydro

A

Grade 1, 2, 3

94
Q

describe grade 1 hydro

A 
mild
slight separation (2 mm) of renal collecting system
95
Q

describe grade 2 hydro

A

moderate
anechoic separation of entire central renal sinus…. pelvis and calyces are dilated

clubbes calyces

96
Q

describe grade 3 hydro

A

severe
thinning of renal cortex w/ extensive enlargement of renal sinus and calyces

loss of calyx definition

97
Q

false + for hydro

A

over distended bladder
extra renal pelvis
multiple parapelvic cysts
AV malformation

98
Q

why is it important to do a post void w/ possible hydro

A

to avoid false +’s

99
Q

another name for renal parenchymal calcium deposits

A

nephrocalcinosis

100
Q

describe renal parenchymal calcium deposits

causes

A

bilateral and diffuse, can be cortical or medullary

ischemia, necrosis or hypercalcemic states

101
Q

US appearance of renal parenchymal calcium deposits

A
  • increased cortical echogenicity
  • echogenic pyramids or walled of pyramids
  • possible shadowing
102
Q

renal parenchymal calcium deposits are difficult to differentiate from which other renal condition

A

medullary sponge kidney

103
Q

describe anderson-carr kidney

A

a high [ ] of calcium in fluid around the tubules that leads to calcium deposits in the margins of the medulla

represents the early development of a stone

104
Q

Us appearance of anderson-carr kidney

A

non-shadowing echogenic rims of renal pyramids

105
Q

describe medical renal disease

what can it cause

A

general term that refers to poorly functioning but un-obstructive kindeys

describes a disease affecting the renal parenchyma (cortex and medulla) bilaterally and diffusely….. can lead to renal failure

106
Q

how do we find the cause of medical renal disease

how is it treated

A

biopsy

medication initially, then surgery

107
Q

areas to evaluate on US w/ medical renal disease

A

renal size and contour
echogenicity
CM junction distinction
renal pyramids and sinus

108
Q

what lab values will be elevated w/ medical renal disease

whats the next step

A

creatinine….. this elevation prompts an US to check for mechanical obstruction… if theres no obstruction this indicates a renal parenchymal abnormality

109
Q

Us appearance of acute medical renal disease

when would the CM junction not be prominent

A

most common: normal

  • varies depending on cause
  • diffuse increase in cortical echogenicity and renal size
  • prominent CM junction

+if the pyramids are affect, CMJ will not be defined

110
Q

US appearance of chronic medical renal disease

A

vary depending on cause

small echogenic kidneys

111
Q

another name for medical renal disease

A

renal parenchymal disease

112
Q

5 causes of medical renal disease

A 
acute tubular necrosis
acute cortical necrosis
acute glomerulonephritis
amyloidosis
diabetes mellitus
113
Q

describe acute tubular necrosis

A

deposits of debris in the renal collecting tubules that can be the result of toxic or ischemic insults (chemo, antibiotics, anti-freeze)

most common cause of acute reversible renal faliure

114
Q

whats the most common cause of acute reversible renal failure

A

acute tubular necrosis

115
Q

US appearance of acute tubular necrosis

how does acute tubular necrosis affect resistance to arterial blood flow

A

usually normal, maybe bilaterally enlarged w/ echogenic pyramids

more resistance, RI >0.75

116
Q

describe acute cortical necrosis

causes

A

ischemic necrosis of the cortex w/ sparing of pyramids…. rare cause of acute renal faliure

sepsis, burns, severe dehydration, preg induced HTN

117
Q

US appearance of acute cortical necrosis

Initial and chronic

A

initially: normal size, hypo cortex and loss of CMJ
chronic: atrophy and cortical calcification

118
Q

describe acute glomerulonephritis

patient presentation

A

an autoimmune rxn

hematuria, HTN, azotemia

119
Q

what is azotemia

another name for azotemia

A

high [ ] of nitrogen containing compounds in the blood

uremia

120
Q

US appearance of acute glomerulonephritis

Early and late

A

early: variable
late: small echogenic kidneys

121
Q

describe amyloidosis

clinical presentation

A

systemic metabolic disorder that leads to amyloid deposits in the kidneys

proteinuria

122
Q

US appearance of amyloidosis

A

variable

123
Q

US appearance of diabetes mellitus

Early and late

A

early: enlarged kidneys
late: small, echogenic, loss of CMJ

124
Q

most common cause of chronic renal failure

A

diabetes mellitus

125
Q

describe renal failure

what does it lead to

treatment

A

inability of kidneys to remove metabolites from blood

azotemia

dialysis (removes waste from kidneys) or renal transplant

126
Q

3 causes of renal failure

describe them

A

pre-renal - sepsis, renal artery stenosis

renal - parenchymal disease

post-renal - obstruction of collecting sys, can be complete or imcomplete

127
Q

if renal obstruction if complete when will irreversible damage occur

incomplete

A

C: 3 wks

IC: 3 months

128
Q

common cause of acute renal failure

is it reversible

A

usually medical renal disease

yes

129
Q

US appearance of acute renal failure

what should you check for

A

usually normal

hydro, obstruction, echogenicity of parenchyma (usually increased)

130
Q

common cause of chronic renal failure

is it reversible

A

diabetes mellitus

no

131
Q

US appearance of chronic renal failure

A

small kidney, echogenic

132
Q

which lab values are increased w/ renal failure

A

serum creatinine (most important and most common)

BUN, uric acid
RBC/WBC in urine
proteinuria

133
Q

describe cushings syndrome

causes

A

results from excess secretion or cortisol

adrenal hyperplasia
adrenal adenoma
adrenal carcinoma
exogenous corticosteroids

134
Q

clinical presentation of cushings

A 
moon face
buffalo hump
truncal obesity (eggs on legs)
hirsutism
amenorrhea
HTN
135
Q

difference b/w cushings syndrome and cushings disease

A

S: due to adrenal abnormality

D: due to pituitary adenoma resulting in too much cortisol

136
Q

describe Conn’s disease

most common cause
other causes

A

excessive aldosterone secretion

adenoma/aldosteronoma (most common)

hyperplasia
carcinoma (uncommon)

137
Q

clinical presentation of Conn’s disease

A

hypernatremia (NA = sodium)
hypokalemia (K = potassium)
HTN

138
Q

US appearance of Conn’s disease

A

small, solid, round mass

hypo

139
Q

describe MEN (multiple endocrine neoplasia) syndrome

where do the tumors usually grow

A
  • tumors develop in several endocrine glands and produce excessive hormones (3 types)
  • can be benign or malignant

adrenal, panc, pituitary, parathyroid

140
Q

type 2 MEN

A
  • autosomal dominant condition w/ malignant pheochromocytomas in the adrenal
  • usually bilateral
141
Q

causes of hypoadrenalism

what can it lead to

A

primary disorders of the adrenal cortex or disorders of the hypothalamus or pituitary

adrenal atrophy

142
Q

causes of addisons disease

A

80% are autoimmune:
these types are chronic, primary hypoadrenalism
affects mostly females

20% due to TB

143
Q

describe addison’s disease caused by TB

clinical presentation

A

affects mostly males
90% of the gland is nonfunctioning

hyperpigmentation
low BP, weakness, fatigue

144
Q

describe waterhous-friderichsen syndrome

causes

A

acute hypoadrenalism that causes massive adernal destruction (big name, big destruction)

hemorrhage, infection

145
Q

treatment for waterhous-friderichsen syndrome

A

glucocorticoid therapy

146
Q

Name for blood in ascites

A

Hemoperitoneum

AB&SS2 (9 decks)

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