38 Liver Disease Flashcards
Hepatocellular Failure
-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
Osteomalacia
softening of the bones
-typically through a deficiency of vitamin D or calcium.
low vitamin K causes
poor blood-clotting factor production
Portal Hypertension
- 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
altered lipoprotein processing
[s/s of hepatocellular failure]
s/s of hepatocellular failure
dyslipidemia: hypertriglyceridemia
inadequate protein metabolism
[s/s of hepatocellular failure]
- decr prodctn of CLOTTING FACTORS
- —-excessive bleeding
- hypoalbuminemia
- —-gen. edema r/t low serum oncotic pressure
MEN’S impaired processing of endogenous steroid hormone
[s/s of hepatocellular failure]
- gynecomastia
- impotence
- testicular atrophy
- fem hair distribution
WOMEN’S impaired processing of endogenous steroid hormone
[s/s of hepatocellular failure]
- irregular menses
- palmar erythema
- spider telangiectasia
impaired clearance of exogenous drugs and toxins
[s/s of hepatocellular failure]
ammonia is converted to urea
JAUNDICE-
PREHEPATIC CAUSE
RBC or spleen issues
-hemolysis, ineffective erythropoiesis
JAUNDICE-
HEPATIC CAUSE
liver
- dysfunction of liver cells
- incr of unconjugated or unconjugated bilirubin
- UDPGT mutations/immature
JAUNDICE-
POSTHEPATIC CAUSE
bile + bile bladder
obstruction of bile ducts, canalicular bilirubin transport, conjugated hyperbilirubinemia
UDPGT
enzyme in liver that converts UNCONJUGATED bilirubin to CONJUGATED
high conjugated bilirubin
sign that liver + blood is working fine.
must be POSTPEHATIC jaundice issue
Portal Hypertension
sluggish perfusion resulting in INCREASED PRESSURE IN PORTAL CIRCULATION
-congested venous drainage of GI tract
Portal Hypertension
s/s
anorexia bc liver cells are not metabolizing
varices (esophageal/gastric/hemorrhoidal can cause rupture>uncontrolled bleeding)
ascites
Gastroesophageal Varices
s/s
- hematemesis (blood in vomit)
- melena (blood in feces)
- brt red rectal bleeding
- anemia
- shock
Gastroesophageal Varices
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
variceal bleeding
life threatening
- 50% mortality
- great risk of rebleed bc the ruptures cause fibrosis, which means low clotting factors
hepatic encephalopathy
treatment
diet: less protein, more carbs, high fiber
- pripheral or central IV infusions
- amoxicillin + rifamixin
ascites occurs with…
portal hypertension + hypoalbuminemia
hepatitis
inflammation of liver parenchyma
-caused by cytomegalovirus or epstein barr
Hep A vs B
A: ssRNA, hepatovirus, fecal-oral, NO chronic liver disease, IgM
B: dsDNA, hepadnavirus, prenatal/sex, 10% chronic liver disease, HBsAg or antibody to it
Hep A [HAV]
aka enteric hepatitis
- fecal-oral
- jaundice,RUQ, malaise, anorexia,
**self limited - lifetime immunity
Anti-HAV IgG vs IgM
presence of anti-HAV IgG = previous infection
IgM = acute infection
HAV treatment
self limiting so supportive
–AVOID ETOH, acetaminophin, hepatotoxin
Hep B
aka serum hepatitis
-parenteral or sexual contact by BLOOOOD
Hep C [HCV]
by flavivirus
-spread thru IV drug use or blood transfusions
most common cause of ESLD
chronic hep C
Cirrhosis
irreversible end-stage of many different hepatic injuries
- liver is fibrotic, scarred, nodular
- results in permanent alteration in hepatic blood flow + liver function
diabetes insipidus
lack of ADH hormone
polyuria
polydipsia
polyphagia
diabetes insipidus
urine quality
3-5 gal/day
low osmolarity
type I vs type II diabetes
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
gestational diabetes
similar to type II “insulin resistant”
-caused by placenta hormone
insulin is synth by….
Beta cell of islet of langerhans in pancreas
alpha cells produce…
glucagon
insulin actions
- enhance protein synth, prevent muscle breakdown
- inhibit gluconeogenesis
- enhance fat deposition
- stim growth
diabetes mellitus
endocrine disorder
chronic hyperglycemia
diabetes mellitus
diagnosis
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
diabetes mellitus
clinical sympt
polys (uria, dipsia, phagia) + losing weight
