Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Year 1: Patho/Pharm > Liver Patho > Flashcards

Liver Patho Flashcards

(52 cards)

Start Studying
1
Q

Definition
Cirrhosis

A

Irreversible inflammation and fibrosis of the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Clinical Signs and Symptoms
Steatosis

A

Asymptomatic
reversible stage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Clinical signs and symptoms
Steatohepatitis

A

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

enlargement of liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Alteration labs
Cirrhosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Pathophysiology
Ascites

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Treatment Liver Disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Treatment
Non alcoholic steatosis

A

behavioural modification
weight loss
diet
exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Definition
Cholithiasis

A

Gallstones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Treatment
Cholelithiasis

A

Transabsominal US

Lithotripsy

Endoscopic removal - ballon dilation

bile salts to dissolve stones (reoccurrence rate high)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Etiology
Cholecystitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Pathophysiology
Cholecystitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Complications of cholecystitis

A

infection
pancreatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Treatment
Cholecystitis

A

removal gallbladder
antibiotics
narcotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Risk Factors
Pancreatitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Levels of pancreatitis

Study These Flashcards
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

Study These Flashcards
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

Study These Flashcards
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

Study These Flashcards
A

malnutrition
weight loss
intermittent abdominal pain
insulin dependence
cancer

25
3 immune cells that line the liver sinusoids
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
Functions of the liver
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
Clinical signs and symptoms Hepatocellular carcinoma
fullness RUQ pain N/V sudden onset anorexia or nausea
28
Types of hepatocellular carcinoma
nodular diffuse massive
29
Risk factors hepatocellular carcinoma
cirrhosis hepatitis B hepatitis C
30
Serology Acute viral hepatitis
HBsAg HBeAg (very infectious) Total Anti-HBc Anti-HBc (IgM) HBV DNA AST, ALT elevated (not correlated with damage) bilirubinemia +
31
Serology Chronic viral hepatitis
HBsAg HBeAg (maybe) Total Anti-HBc Anti-HBc (IgG) Anti-HBe (chronic infection under control) HBV DNA
32
Serology HB vaccination
Anti-HBs
33
Recovered and HBV immune
anti-HBs Total anti-HBc
34
Confounding HBV serology
Biotin - false positive or negative HBV within 18 days of serology can yield + HBsAg (re-testing required) 180 day window
35
Hepatitis B transmission
blood needles unprotected sex not usually saliva, unless broken skin pregnancy
36
Hepatitis B Screening
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
How is HBV similar and different from HIV
reverse transcripts = high mutation rate anti-virals evades vaccination for HBV 90% people clear HBV 0% clear HIV
38
Definitions serology
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
Most common cause of ascites
cirrhosis 25% mortality
40
Most common cause of hepatocellular carcinoma
HBV or HCV cirrhosis
41
Type 2 DM Risk factors
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
Insulin receptor sensitivity Influenced by...
Age weight exercise stress BP dyslipidemia *the risk factors for Type 2 DM
43
Type 2 DM Clinical signs and symptoms
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 >> - hyperglycemia >> - albuminuria - glucosuria - electrolyte imbalances: hyponatremia, hypokalemia - blurred vision - fatigue - infections, impaired wound healing - cardiovascular symptoms
44
Type 2 DM Pathophysiology
Genetics x environment 1. increased insulin resistance - obesity (adipokines, cytokines) - decrease grhelin 2. insulin hypersecretion - increased demand - leads to beta cell dysfunction - adipokines are also cytotoxic to beta cells directly 3. silent hyperglycemia - cells have enough insulin to take up glucose - masked hyperglycemia - microvascular and macrovascular damage from glucose 4. 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 5. Counter-regulatory hormone glucagon negative inhibition (insulin, amylin) removed - increase breakdown of fat, muscle, glycogen stores - increase blood glucose
45
Type 2 DM Screening
Early screening if risk factors present (metabolic syndrome) >/= 40 years every 3 years Every 6-12 months if risk factors present CANRISK calculator
46
Gestational DM Prevalence
3-20% of pregnancies *screen all pregnancies at 24 weeks
47
Gestational DM Risk Factors
- 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
Gestational DM Clinical manifestations
1. Silent hyperglycemia - screen everyone at 24 weeks 2. Symptomatic - polyuria, polydipsia, polyphagia, fatigue, weight loss
49
Gestational DM Preferred vs. Alternate screening
1. 50g oral glucose tolerance test - 2 hour mark 9mmol/L Followed by 2. 75g oral glucose tolerance test - 2 hour mark 8.5 mmol/L (normal > 11.1mmol/L) *lower threshold as baby takes up glucose
50
Gestational DM Complications of hyperglycemia
- still birth - spontaneous abortions - pre-eclampsia - congenital abnormalities (teratogenic) - retinopathy *tighter glycemic controls in pregnancy Hypoglycemia < 3.7mmol/L A1C target < 6.1%
51
Gestational DM Pathophysiology
- 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
Gestational DM Patient education Post-partum
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 (45 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions