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Year 1: Patho/Pharm > Liver Patho > Flashcards

Liver Patho Flashcards

1
Q

Definition
Cirrhosis

A

Irreversible inflammation and fibrosis of the liver

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2
Q

Etiology
Cirrhosis

A

Top 3
1. Hepatitis virus (HBV, HCV)
2. alcohol
3. idiopathic

Others
- metabolic
- autoimmune
- toxins/chemicals
- venous obstruction (R sided heart failure)

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3
Q

Stages of Liver disease

A
  1. Steatosis (fatty liver)
    - increase deposition TG / fat in liver
    - increase lipogenesis (TG, FFA, cholesterol)
    - decrease FA oxidation
    - Asymptomatic
  2. Steatohepatitis
    - Kupffer cells: macrophages, phagocytosis, inflammation, recruitment WBC
    - Mallory Dank Bodies: myofibroblasts, irreversible fibrosis
  3. Cirrhosis
    - inflammation
    - death of hepatocytes
    - loss of liver function
    - hepatorenal failure
    - hepatic portal hypertension
    - hepatic encephalopathy
    - death
    - ascites
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4
Q

Clinical Signs and Symptoms
Steatosis

A

Asymptomatic
reversible stage

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5
Q

Clinical signs and symptoms
Steatohepatitis

A

irreversible inflammation: fever, nausea, vomiting, anorexia, fatigue

enlargement of liver

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6
Q

Clinical Signs and Symptoms
Cirrhosis

A

decreased synthesis of plasma proteins: decreased oncotic pressure, decreased albumin, ascites

Decreased metabolism fats, carbs: hypoglycaemia

decreased metabolism of bilirubin and obstruction bile: hyperbilirubenemia, jaundice, dark urine, pale stools

portal hypertension: ascites, varices, hemorrhoids, thrombocytopenia, leukopenia, anemia, splenomegaly

Ascites: inflammation, permeability, lymph, GI leak, RAS activation, portal hypertension

hepatorenal failure

hepatoencephalopathy

Bleeding: decreased absorption vitamin K, splenomegaly

Alterations of labs detectable

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7
Q

Alteration labs
Cirrhosis

A

elevated AST, ALT, ALP
bilirubinemia
BUN
low albumin
increased PTT

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8
Q

Pathophysiology
Ascites

A

portal vein hypertension
inflammation
Translocation gut bacteria
RAAS pathway activation
lymph
low oncotic pressure/low albumin

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9
Q

Treatment Liver Disease

A

No treatment
Symptom support
- drain ascites
- corticosteroids - supresison inflammation
- liver transplant

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10
Q

Risk Factors
Non alcoholic fatty liver disease (NAFLD)
Non alcoholic steatosis

A

obesity
type II DM
metabolic syndrome
Dyslipidemia (high TG, high cholesterol)

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11
Q

Treatment
Non alcoholic steatosis

A

behavioural modification
weight loss
diet
exercise

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12
Q

Definition
Cholithiasis

A

Gallstones

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13
Q

3 types of Gallstones

A
  1. Cholesterol stones
    > 70% cholesterol
    calcium
    phosphate
    bile acids
    bilirubin
    mucin
  2. Brown stones
    bacterial or parasitic infection
    calcium carbonate
    fatty acid soaps
  3. Black stones
    mucin + calcium carbonate
    hemorrhage
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14
Q

Clinical Manifestations
Cholelithiasis

A

Asymptomatic

RUQ pain
intolerance fatty foods, cabbage
heart burn, flatulence

Biliary colic
30 minutes after eating fatty food
RUQ pain
radiation upper / middle back
lodge stone in common bile duct
jaundice

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15
Q

Treatment
Cholelithiasis

A

Transabsominal US

Lithotripsy

Endoscopic removal - ballon dilation

bile salts to dissolve stones (reoccurrence rate high)

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16
Q

Etiology
Cholecystitis

A

Inflammation of gallbladder caused by obstruction of common bile duct by gallstone

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17
Q

Pathophysiology
Cholecystitis

A

Obstruction common bile duct
back up bile into gallbladder
pressure results in ischemia
inflammation and necrosis
perforation gallbladder

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18
Q

Complications of cholecystitis

A

infection
pancreatitis

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19
Q

Treatment
Cholecystitis

A

removal gallbladder
antibiotics
narcotics

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20
Q

Risk Factors
Pancreatitis

A

Black
Alcohol, smoking
Dyslipidemia, obesity
Genetics
PUD, trauma
Medications
Unknown

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21
Q

Levels of pancreatitis

A
  1. Acute pancreatitis
    - mild
    - resolves on own
  2. Obstructive pancreatitis
    - severe
    - hospitalization
    - debilitating epigastric pain
    - radiation to back
  3. Chronic pancreatitis
    - Chronic pancreas inflammation
    - progressive fibrosis of the pancreas
    - destruction acinar cells and islet of langerhans
22
Q

Pathophysiology
Pancreatitis

A
  1. Direct damage
    Example. Alcohol
    Direct damage to acinar cells
    inflammatory response
    activates lytic enzymes (lipases, elastases, trypsin) resulting in auto digestion
    formation coagulation necrosis, fat necrosis, pseudocyts
    ischemia and necrosis
    Systemic symptoms
  2. obstruction
    example. cholelithiasis
    obstruction common duct
    back up of pancreatic juices
    pressure leads to ischemia, inflammation, necrosis
    activation enzymes leads to auto digestion
    coagulation necrosis, fat necrosis, pseudocysts
    Systemic symptoms
23
Q

Clinical Signs and Symptoms
obstructive pancreatitis

A

medical emergency

  1. severe debilitating epigastric pain
  2. radiation to back

Inflammation, mass release inflammatory mediators
N/V/fever
hypotension and shock
decreased cardiac output leads to acidosis
activation coagulation and bleeding (DIC)
multiorgan failure
ARDs
Renal failure (ATN)
GI peristalsis, bleeds
translocation bacteria, ascites and sepsis

24
Q

Clinical Signs and Symptoms
Chronic pancreatitis

A

malnutrition
weight loss
intermittent abdominal pain
insulin dependence
cancer

25
Q

3 immune cells that line the liver sinusoids

A
  1. Kupffer cells
    - macrophages
    - lipid metabolism
    - bilirubin production
    - healing
  2. stellate cells
    - vitamin A
    - APC
    -EPO
    - trap bacteria
    - contractile
    - myofibrobalsts
  3. NK cells
    - tumor defence
26
Q

Functions of the liver

A
  1. Bile
    - absorption of fat
  2. synthesis carrier proteins, clotting factors, albumin, immunoglobulins
    - oncotic pressure and BP
    - coagulation
  3. gluconeogenesis, glycogenesis, glycogenolysis
    - regulation blood glucose
    - glycogen stores
    - keto acids produced when a.a deaminated
  4. lipogenesis, liopolysis
    - cholesterol, phospholipids
    - cell membranes and steroid hormones
  5. EPO
  6. detoxify
27
Q

Clinical signs and symptoms
Hepatocellular carcinoma

A

fullness
RUQ pain
N/V
sudden onset anorexia or nausea

28
Q

Types of hepatocellular carcinoma

A

nodular
diffuse
massive

29
Q

Risk factors hepatocellular carcinoma

A

cirrhosis
hepatitis B
hepatitis C

30
Q

Serology Acute viral hepatitis

A

HBsAg
HBeAg (very infectious)
Total Anti-HBc
Anti-HBc (IgM)
HBV DNA
AST, ALT elevated (not correlated with damage)
bilirubinemia +

31
Q

Serology Chronic viral hepatitis

A

HBsAg
HBeAg (maybe)
Total Anti-HBc
Anti-HBc (IgG)
Anti-HBe (chronic infection under control)
HBV DNA

32
Q

Serology HB vaccination

A

Anti-HBs

33
Q

Recovered and HBV immune

A

anti-HBs
Total anti-HBc

34
Q

Confounding HBV serology

A

Biotin - false positive or negative

HBV within 18 days of serology can yield + HBsAg (re-testing required)

180 day window

35
Q

Hepatitis B transmission

A

blood
needles
unprotected sex
not usually saliva, unless broken skin
pregnancy

36
Q

Hepatitis B Screening

A

pregnancy
HIV infections/HCV infections (common mode of transmission)
prison/institutions
occupational health
immunocompromised
immunosuppressive therapy
high risk sexual activities
needle sharing
positive mother
endemic country

37
Q

How is HBV similar and different from HIV

A

reverse transcripts = high mutation rate
anti-virals evades

vaccination for HBV

90% people clear HBV 0% clear HIV

38
Q

Definitions
serology

A

HBsAg - active, acute/chronic infection, surface

HbeAg - active infection, secreted hepatocytes, infectious high

Total anti-HBc
IgM - acute infection
IgG - chronic infection

Anti-HBe
chronic infection under immune control

Anti-HBs
recovery, immunity present

HBV DNA
viral load of DNA

39
Q

Most common cause of ascites

A

cirrhosis
25% mortality

40
Q

Most common cause of hepatocellular carcinoma

A

HBV or HCV
cirrhosis

41
Q

Type 2 DM
Risk factors

A

Obesity *primary driver

Metabolic syndrome
- waist circumference
- HTN
- dyslipidemia
- hyperglycemia

Pre-diabetes
- impaired FPG 6.1-6.9
- impaired A1C 6.0-6.4
- impaired GTT 7.8-11.0

Male

Age > 40 years

Ethnic minority

PCOS

Sleep apnea

Neuropsychiatric diseases (Drug related)

NAFLD (metabolic syndrome correlation)

42
Q

Insulin receptor sensitivity
Influenced by…

A

Age
weight
exercise
stress
BP
dyslipidemia

*the risk factors for Type 2 DM

43
Q

Type 2 DM
Clinical signs and symptoms

A

Silent hyperglycemia
- masked by hypersecertion of insulin by beta cells
- microvascular and macrovascular complications (very damaging)

Same clinical signs and symptoms as type 1 DM except:
- no ketoacidosis
- not underweight
- no C-peptide
- no auto-antibodies (IA-2A, anti-GABA)

Clinical Signs and Symptoms
- polyuria, polydipsia, polyphagia
- hyperosmolality&raquo_space;
- hyperglycemia&raquo_space;
- albuminuria
- glucosuria
- electrolyte imbalances: hyponatremia, hypokalemia
- blurred vision
- fatigue
- infections, impaired wound healing
- cardiovascular symptoms

44
Q

Type 2 DM
Pathophysiology

A

Genetics x environment

  1. increased insulin resistance
  • obesity (adipokines, cytokines)
  • decrease grhelin
  1. insulin hypersecretion
  • increased demand
  • leads to beta cell dysfunction
  • adipokines are also cytotoxic to beta cells directly
  1. silent hyperglycemia
  • cells have enough insulin to take up glucose
  • masked hyperglycemia
  • microvascular and macrovascular damage from glucose
  1. beta cell dysfunction
  • adipokines cytotoxicity to beta cells
  • insulin resistance increased production demand
  • resistance to incretins (GLP1 and GIP from GI)
  • decreased insulin production
  • decreased amylin production
  • results in 1. increase blood glucose 2. decreased saeity 3. increased GI motility
  • increases glucagon secretion
  1. Counter-regulatory hormone

glucagon negative inhibition (insulin, amylin) removed
- increase breakdown of fat, muscle, glycogen stores
- increase blood glucose

45
Q

Type 2 DM
Screening

A

Early screening if risk factors present
(metabolic syndrome)

> /= 40 years every 3 years

Every 6-12 months if risk factors present

CANRISK calculator

46
Q

Gestational DM
Prevalence

A

3-20% of pregnancies

*screen all pregnancies at 24 weeks

47
Q

Gestational DM
Risk Factors

A
  • obesity
  • ethnic minorities
  • age
  • family history
  • PCOS
  • pre-diabetes prior to pregnancy (metabolic syndrome prior to pregnancy)

*80% have underlying beta cell dysfunction/insulin resistance prior to pregnancy

48
Q

Gestational DM
Clinical manifestations

A
  1. Silent hyperglycemia
    - screen everyone at 24 weeks
  2. Symptomatic
    - polyuria, polydipsia, polyphagia, fatigue, weight loss
49
Q

Gestational DM
Preferred vs. Alternate screening

A
  1. 50g oral glucose tolerance test
    - 2 hour mark 9mmol/L

Followed by

  1. 75g oral glucose tolerance test
    - 2 hour mark 8.5 mmol/L (normal > 11.1mmol/L)

*lower threshold as baby takes up glucose

50
Q

Gestational DM
Complications of hyperglycemia

A
  • still birth
  • spontaneous abortions
  • pre-eclampsia
  • congenital abnormalities (teratogenic)
  • retinopathy

*tighter glycemic controls in pregnancy

Hypoglycemia < 3.7mmol/L
A1C target < 6.1%

51
Q

Gestational DM
Pathophysiology

A
  • 80% individuals have underlying beta cell dysfunction (decreased insulin, amylin, response to incretins) and insulin resistance (adipokines)

Placental hormones increase insulin resistance
- GH, cortisol, estrogen, progesterone, lactogen
- increase glucose availability for fetus

beta cell hyperplasia, hypertrophy
- increase insulin secretion
- for fetal uptake

Increased counter-regulatory hormone production by mom
- glucagon
- cortisol

52
Q

Gestational DM
Patient education Post-partum

A

Breast feed immediately and minimum 4 months
- prevent diabetes mom and child
- prevent hypoglycemia neonate

Diabetes screen 6 weeks and 6 months

Monitoring for post-partum thyroiditis

Year 1: Patho/Pharm (39 decks)

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