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Pathophysiology > 38 Liver Disease > Flashcards

38 Liver Disease Flashcards

1
Q

Hepatocellular Failure

A

-jaundice
-decr clotting factor>excess bleed
-hypoalbuminemia
-decr vit D, K
-feminization
-osteomalacia
-lack of bile production>impaired absorption of fat soluble vitamins (ADEK)
-abnormal storage/release of glucose
hyper/hypoglycemia

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2
Q

Osteomalacia

A

softening of the bones

-typically through a deficiency of vitamin D or calcium.

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3
Q

low vitamin K causes

A

poor blood-clotting factor production

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4
Q

Portal Hypertension

A
  • GI congestion
  • dvlpt of esophageal or gastric varices
  • hemorrhoids
  • splenomegaly
  • ascites
  • inadequate protein metabolism
  • impaired processing of endogenous steroid hormone
  • impaired clearance of exogenous drugs + toxins
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5
Q

altered lipoprotein processing

[s/s of hepatocellular failure]

A

s/s of hepatocellular failure

dyslipidemia: hypertriglyceridemia

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6
Q

inadequate protein metabolism

[s/s of hepatocellular failure]

A
  • decr prodctn of CLOTTING FACTORS
  • —-excessive bleeding
  • hypoalbuminemia
  • —-gen. edema r/t low serum oncotic pressure
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7
Q

MEN’S impaired processing of endogenous steroid hormone

[s/s of hepatocellular failure]

A
  • gynecomastia
  • impotence
  • testicular atrophy
  • fem hair distribution
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8
Q

WOMEN’S impaired processing of endogenous steroid hormone

[s/s of hepatocellular failure]

A
  • irregular menses
  • palmar erythema
  • spider telangiectasia
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9
Q

impaired clearance of exogenous drugs and toxins

[s/s of hepatocellular failure]

A

ammonia is converted to urea

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10
Q

JAUNDICE-

PREHEPATIC CAUSE

A

RBC or spleen issues

-hemolysis, ineffective erythropoiesis

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11
Q

JAUNDICE-

HEPATIC CAUSE

A

liver

  • dysfunction of liver cells
  • incr of unconjugated or unconjugated bilirubin
  • UDPGT mutations/immature
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12
Q

JAUNDICE-

POSTHEPATIC CAUSE

A

bile + bile bladder

obstruction of bile ducts, canalicular bilirubin transport, conjugated hyperbilirubinemia

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13
Q

UDPGT

A

enzyme in liver that converts UNCONJUGATED bilirubin to CONJUGATED

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14
Q

high conjugated bilirubin

A

sign that liver + blood is working fine.

must be POSTPEHATIC jaundice issue

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15
Q

Portal Hypertension

A

sluggish perfusion resulting in INCREASED PRESSURE IN PORTAL CIRCULATION
-congested venous drainage of GI tract

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16
Q

Portal Hypertension

s/s

A

anorexia bc liver cells are not metabolizing
varices (esophageal/gastric/hemorrhoidal can cause rupture>uncontrolled bleeding)
ascites

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17
Q

Gastroesophageal Varices

s/s

A
  • hematemesis (blood in vomit)
  • melena (blood in feces)
  • brt red rectal bleeding
  • anemia
  • shock
18
Q

Gastroesophageal Varices

A

venous network in proximal stomach + esophagus can rupture at high pressure

—collateral venous pathway (surrounds the main venous network) will dilate in response to elevated portal pressure

-half of cirrhotic patients

19
Q

variceal bleeding

A

life threatening

  • 50% mortality
  • great risk of rebleed bc the ruptures cause fibrosis, which means low clotting factors
20
Q

hepatic encephalopathy

treatment

A

diet: less protein, more carbs, high fiber
- pripheral or central IV infusions
- amoxicillin + rifamixin

21
Q

ascites occurs with…

A

portal hypertension + hypoalbuminemia

22
Q

hepatitis

A

inflammation of liver parenchyma

-caused by cytomegalovirus or epstein barr

23
Q

Hep A vs B

A

A: ssRNA, hepatovirus, fecal-oral, NO chronic liver disease, IgM

B: dsDNA, hepadnavirus, prenatal/sex, 10% chronic liver disease, HBsAg or antibody to it

24
Q

Hep A [HAV]

A

aka enteric hepatitis

  • fecal-oral
  • jaundice,RUQ, malaise, anorexia,

**self limited - lifetime immunity

25
Q

Anti-HAV IgG vs IgM

A

presence of anti-HAV IgG = previous infection

IgM = acute infection

26
Q

HAV treatment

A

self limiting so supportive

–AVOID ETOH, acetaminophin, hepatotoxin

27
Q

Hep B

A

aka serum hepatitis

-parenteral or sexual contact by BLOOOOD

28
Q

Hep C [HCV]

A

by flavivirus

-spread thru IV drug use or blood transfusions

29
Q

most common cause of ESLD

A

chronic hep C

30
Q

Cirrhosis

A

irreversible end-stage of many different hepatic injuries

  • liver is fibrotic, scarred, nodular
  • results in permanent alteration in hepatic blood flow + liver function
31
Q

diabetes insipidus

A

lack of ADH hormone
polyuria
polydipsia
polyphagia

32
Q

diabetes insipidus

urine quality

A

3-5 gal/day

low osmolarity

33
Q

type I vs type II diabetes

A

i: “INSULIN DEPENDANT” beta cells on pancreas are defected> DECR in insulin production > less uptake of blood glucose
- –autoimmune disease

ii: “INSULIN RESISTANT” normal level of insulin BUT issues w receptor binding/signaling. cannot take insulin> less uptake of blood glucose

34
Q

gestational diabetes

A

similar to type II “insulin resistant”

-caused by placenta hormone

35
Q

insulin is synth by….

A

Beta cell of islet of langerhans in pancreas

36
Q

alpha cells produce…

A

glucagon

37
Q

insulin actions

A
  • enhance protein synth, prevent muscle breakdown
  • inhibit gluconeogenesis
  • enhance fat deposition
  • stim growth
38
Q

diabetes mellitus

A

endocrine disorder

chronic hyperglycemia

39
Q

diabetes mellitus

diagnosis

A

2 of the following:

  • blood glucose above 200 mg/dl
  • fasting bld gluc lvl>126mg/dl
  • 75g oral glucose load>2 hrs>bld gluc lvl>126
  • HgbA1C lvl above 6.5
40
Q

diabetes mellitus

clinical sympt

A

polys (uria, dipsia, phagia) + losing weight

Pathophysiology (32 decks)

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