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Gastroenterology Dx > Midterm 2 > Flashcards

Midterm 2 Flashcards

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1
Q

hepatitis

A

inflammation of the liver w/ change of its function

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2
Q

hepatitis - has 2 forms

A

1) acute – lasts less than 6 months
2) chronic – lasts more than 6 months
- –NB asks about acute & chronic hepatitis—

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3
Q

hepatitis is caused by which type of DNA?

A

RNA (ribonucleic acid)

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4
Q

hepatitis 1) viral - 2 types

A

HAV – +ssRNA (infectious hepatitis)

HBV – +dsDNA (serum hepatitis)

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5
Q

hepatitis HAV (viral)

A

hepatitis HAV - +ssRNA (infectious hepatitis)

  • spreads through fecal contaimination of food & water
  • causes acute & self-limiting infection
  • does NOT cause chronic hepatitis
  • ONLY ACUTE
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6
Q 
hepatitis HBV (viral)
*most common*
A

hepatitis HBV - +dsRNA (serum hepatitis) most common

  • spreads through blood, bodily fluids, sexual contacts, tattoos, mother to child by breast feeding
  • causes acute & self-limiting infection
  • causes chronic hepatitis
  • can cause cirrhosis & cancer
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7
Q

NB - What is the most common Dx in later stages of non-A, non-B Hepatitis?

A

hepatitis HCV - +ssRNA (serum non-A, non-B hepatitis)

  • spreads through:
  • sexual contacts
  • hemotransfusions
  • cross the placenta
  • acute & chronic
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8
Q

hepatitis HCV (viral)

A

hepatitis HCV - +ssRNA (serum non-A, non-B hepatitis)

  • spreads through:*
  • sexual contact
  • hemotransfusions
  • crosses the placenta

Acute & Chronic forms

most common causes:

  • chronic hepatitis
  • cirrhosis
  • liver cancer
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9
Q

hepatitis HDV (viral)

A

hepatitis HDV- -ssRNA (serum delta hepatitis)

  • most aggressive form
  • high mortality rate
  • cannot exist w/o B virus
  • spreads through:*
  • blood *
  • typical for I.V. drug users
  • typical for hemophilia pts.

most common causes:

  • chronic hepatitis
  • cirrhosis
  • liver cancer

*ONLY 50% survive Hep. HDV

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10
Q

hepatitis HEV - +ssRNA (infectious hepatitis)

A 
hepatitis HEV - +ssRNA (infectious hepatitis)
*spreads through*
 - contaminated food & water
 - dirty fingers on food
 - ONLY ACUTE FORM
 - often causes acute & self-limiting infection
(unlike hepatitis A) causes: 
 - severe intralobular necrosis
 - acute cholangitis
NO CHRONIC hepatitis
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11
Q

hepatitis HFV - (serum mutated B-virus)

A 
hepatitis HFV - (serum mutated B-virus)
spreads through:
 - blood transfusion
 - oral fecal route
 - body fluid
*causes CHRONIC hepatitis*
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12
Q

hepatitis HGV (GB virus C)

A

hepatitis HGV (GB virus C)
spreads through:
- blood
- sexual contact
*does not appear to replicate primarily in liver
- characteristics are in process of study

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13
Q

hepatitis incubation period

A 
hepatitis A— 28 days (15-50 days)
hepatitis B — 90 days (30-150 days)
hepatitis C — 50 days (15-160 days)
hepatitis D — 60-90 days (30-180 days)
hepatitis E — 40 days (14-60 days)
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14
Q

Cytomagalovirus

A

Cytomagalovirus - DVA

- Type V Hypersensitivity rxn

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15
Q

Epstein-Barr virus

A

Epstein-Barr virus

  • Type IV Hypersensitivity rxn
  • mononucleosis
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16
Q

Yellow fever virus

A

Yellow fever virus

  • yellow color skin
  • destroys liver, etc.
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17
Q

herpes simplex virus

A

Type I hypersensitivity rxn

most common type

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18
Q

ebola virus & Marburg virus

A

ebola virus & Marburg virus:

  • *dangers to pregnant women
  • destroys baby fetus
  • all organs & RBC destroyed
  • destruction of RBC
  • multiple bleedings
    • Marburg*
  • development of hepatitis 2 - Acute hepatitis
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19
Q

Herpes Zoster

A

Herpes Zoster

- Type III hypersensitivity rxn

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20
Q

hepatitis Etiology: #2

A

hepatitis etiology: #2
2) toxic hepatitis:
caused by:
- medications (e.g. Tylenol, birth control pills, Lipitor, etc)
- medication most common factor
- long time tx w/ more than 6 months
– mushroom poison
– alcohol (most common cause of TOXIC hepatitis)
Lipitor - destruction of hepatocytes (hepatitis)
* can happen from 1-time consumption of alcohol

Toxic shock - multiple organs involved

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21
Q

hepatitis Etiology: #3

A

hepatitis Etiology: #3

3) bacteria, e.g.
- staphylococci & streptococci bacteria
- causes Toxic Shock Syndrome (TSS)
- leptospira (Gram-negative spirochaete)
- listeria (Gram-positive, non spore-forming, rods)

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22
Q

hepatitis Etiology: #4

A

hepatitis Etiology: #4

4) protozoa, e.g.:
- Toxoplasma -
• most common for fetus
• destroys fetus
• pregnant women - should not touch ANY animal while pregnant
- Leishmania

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23
Q

hepatitis Etiology: #5

A

hepatitis Etiology: #5

5) parasite, e.g.:
- Echinococcus
- 70% in liver
• also in pancreas & lungs
• 1 large cyst produces toxic fluid
• looks like honey cumb
* mechanical destruction of hepatocytes:
- 1. mechanical
- 2. chemical destruction

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24
Q

hepatitis Etiology: #6

A

hepatitis Etiology: #6

6) parasites, e.g.:
 • Toxocara
 • Shistosoma
 —most common in small veins 
— abscess & rupture
— bleeding & destruction of tissue
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25
hepatitis Etiology: #7
hepatitis Etiology: #7 7) fungi, e.g. • Aspergillus - NB - cancer of the liver, very hard for Tx • Histoplasma capsulatum • Candida - yeast, candida abicans - usually chronic hepatitis — dev. cancer of liver when chronic
26
hepatitis Etiology: #8
hepatitis Etiology: #8 8) autoimmune diseases, e.g.: • Sjögren's syndrome - autoimmune disorder> destruction of CT --> exopthalmus, exo...
27
hepatitis Etiology: #9
hepatitis Etiology: #9 9) obesity (non-alcoholic steatosisi) • fat accumulates in hepatocytes
28
hepatitis Etiology: #10
hepatitis Etiology: #10 10) genetic causes of hepatitis: • alpha -1-antitrypsin deiciency (abnormal accumulation of the protein w/i liver cells • hemochromatosis (iron accumulates in multiple body sites, including the liver) — also in brain, heart, lung, kidney • wilson disease (copper accumulates in the liver & brain) — genetic disorder---chronic • glycogen storage disorders – pts. now can live up to 50 years w/tx
29
hepatitis Etiology: #11
hepatitis Etiology: #11 ``` 11) ischemic hepatitis (or shock liver) • most often associated with: – heart failure – shock – sepsis ```
30
hepatitis C is known as what?
'the silent killer' | – may not know you have it for up to 8 months
31
hepatitis signs & symptoms
hepatitis signs & symptoms: – varies according to acute or chronic & etiologic factor – multiple ages, gender
32
hepatitis chronic
hepatitis chronic: C – initial manifestations - cause long-term disease – hep C dev. chronic w/o acute form
33
hepatitis acute
hepatitis acute: E & A - acute only | – initial manifestations of hepatitis may start & get better quickly
34
viral, bacterial, fungal, and toxic etiological agents, usually result in:
viral, bacterial, fungal, and toxic etiological agents, usually result in: — acute hepatatis w/ further progression to chronic hepatitis (except HAVa & HEV)
35
autoimmune, parasites, protozoa, obesity, genetic, ischemic etiological agents usually result in:
autoimmune, parasites, protozoa, obesity, genetic, ischemic etiological agents usually result in: – progression to chronic hepatits
36
initial manifestations of acute hepatitis for first 2-4 days are non-specific, and characterized by flu-like signs & symptoms:
``` initial manifestations of acute hepatitis for first 2-4 days are non-specific, and characterized by flu-like signs & symptoms: – fever – malaise – joint aches – headache – nausea, vomiting – diarrhea ```
37
what are the typical signs & symptoms for acute hepatitis in overt stage?
what are the typical signs & symptoms for acute hepatitis in overt stage? – hepatomegaly (increased size liver - nociceptors never present in liver normally - distention of capsule may cause pain) – abnormal discomfort & pain – jaundice - yellowing of the skin & eyes (icterus) – lymphadenopathy – dark colored urine – white stool
38
what does chronic hepatitis usually result from?
what does chronic hepatitis usually result from? – acute form of hepatitis, but sometimes develops insidiously, w/ non-specific initial clinical manifestations – no specific clinical presentation – pt. feels tired all day – fatigue & weakness
39
what signs & symptoms are typical for all forms & etiologies of hepatitis in overt stage?
what signs & symptoms are typical for all forms & etiologies of hepatitis in overt stage? – weight loss (more than 10lbs in month) – easy bruising (bruising w/o trauma - decreases fxn in liver--> acute form of hepatitis--->remove medications & liver improves – encephalopathy – hepatosplenomegaly – dark stool – dark urine - direct bilirubin – blocking technique helpful (non-Hodgkins = painless)
40
hepatitis dx: tests for bilirubin
hepatitis dx: tests for bilirubin – considerable increase of blood total & conjugated (direct) bilirubin – finding of bilirubin in urine (resulting in dark brown color of urine, like dark beer) * – increased concentration of urobilirubinogen in urine
41
hepatitis dx: blood tests (3 types)
hepatitis dx: blood test (3 types) 1. liver enzymes aka aminotransferases – measures of liver homeostasis (liver panel - multiple enzymes present) – their high concentrations develop as a result of destruction or inflammation not only in liver, but other tissues
42
hepatitis dx: blood tests: 1) aminotransferases
hepatitis dx: blood tests: 1) aminotransferases – Aspartate aminotransferase (AST) – Alanine aminotransferases (ALT) – Gamma glutamyltransferase (GGT)
43
hepatitis dx: blood tests: 1) aminotransferase a) AST
hepatitis dx: blood tests: 1) aminotransferase a) aspartate aminotrasferase (AST) – aka 'serum glutamic oxalocetic transaminase' (SGOT) is intracellular enzymes AST blood concentration - significant increases: – acute toxic hepatitis – acute viral hepatitis – alcoholic liver disease
44
hepatitis dx: blood tests: 1) aminotransferase a) AST (cont'd)
hepatitis dx: blood tests: 1) aminotransferase a) aspartate aminotrasferase (AST) (cont'd) – aka 'serum glutamic oxalocetic transaminase' (SGOT) ``` – present in liver and: • skeletal muscles • heart muscle • brain • lungs • pancreas *it can be released from these tissues in the case of their destruction ``` *AST present for 6 hrs after myocardial infarction
45
hepatitis dx: blood tests: 1) aminotrasferase b) alanine aminotransferase (ALT) aka 'serum glutamic pyruvic transaminase (SGPT) - intracellular enzymes
ALT is normally most concentrated in liver cells - lesser degree - in the heart muscle cells, kidneys, pancrease its blood elevation is significantly increased in case of acute hepatocyte destruction, or severe heart kidneys, pancreas damage
46
hepatitis dx: blood tests: 1) aminotrasferase | c) gamma-glutamyltransferase (GGT)
found: hepatobiliary cells membranes - also in cell membranes of other tissues ex: kidneys, heart, brain ``` GGT blood concentration: — significantly increased in liver diseases assoc with: hepatocyte necrosis cirrhosis alcoholic liver disease ```
47
hepatitis dx: 2) anti-viral antibodies & viral genetic materials
helpful in diagnosis of both acute & chronic hepatitis 1) anti-HAV (for hep A) 2) anti-HBV (for hep B) - 3 tests for B 3) anti-HCV (for hep C)
48
hepatitis dx: 3) serum proteins - IgM, IgG
IgM - indicates acute case -----(NB - IgM synthesized 1st in baby) IgG - indicates chronic case -----(passes through placenta)
49
hepatitis dx: 3) serum proteins - hypoalbuminemia
hypoalbuminemia - indicates a decreased fxn of hepatocytes | - prognosis: decreased production of albumins - oncotic pressure - liquid inside of the veesels, edema
50
hepatitis dx: 3) seurm proteins - | increased prothrombin time
indicates the decreased production of clotting factors
51
what are the most specific tests for hypoalbuminemia?
hypoalbuminemia | increased prothrombin time
52
hepatitis dx:
III. ultrasound - chronic or cancer of liver | IV. liver biopsy - only present w/ chronic hepatitis
53
hepatitis complications:
* liver cirrhosis (hepatitis B, C, D, F, toxic, autoimmune, genetic) * hepatic failure: may dev in pts w/ hep C (hepatoma) * hepatocellular carcinoma (hepatoma)
54
what percentage of chronic hepatitis pts will develop liver cirrhosis?
25%
55
what percentage of patients with liver cirrhosis develop liver cancer each year?
3-5%
56
hepatitis tx:
*medical, depends on the cause of hepatitis rec by chiro: – rest to minimize energy demands – avoid alcohol & other hepatotoxic drugs (e.g. Tylenol) – small amount, high-calorie meal (important for healing) *never ever recommend to use Tylenol or any other medication
57
liver cirrhosis
consequence of chronic liver diseases characterized by replacement of liver tissue by scarring tissue leading to loss of liver function ``` scar tissue is fibrotic tissue - changes structure & fxn - fxn of organ decreases - no more than 6 mm examination: - Arm on R sige - R arm start from belly button - inhale, move fingers down - must have organ between two fingers ```
58
liver cirrhosis etiology
alcoholism major etiological factor 16-40---cirrhosis of liver
59
Stages of Alcoholic Liver disease
1. Healthy liver 2. Fatty liver - deposits of fat lead to liver enlargement 3. Liver Fibrosis - scar tissue forms 4. Cirrhosis - growth
60
Stages of Alcoholic Liver disease
1. Healthy liver 2. Fatty liver - deposits of fat lead to liver enlargement 3. Liver Fibrosis - scar tissue forms 4. Cirrhosis - growth of connective tissue destroys liver cells
61
alcoholic steatosis - "fatty liver"
accumulation of fat in the hepatocytes, may result in altered fat metabolism in liver & increase synthesis of fatty acids & triglycerides. enlargement of the liver is accompanied by symptoms - anorexia - nausea - jaundice * fatty changes @ this point are generally reversible if alcohol consumption ceases
62
mallory bodies
- eosinophilic cytoplasmic inclusion - alcoholic hyaline - found in liver cells * NB - alcoholism & cirrhosis questions
63
liver cirrhosis etiology
non-alcoholic steatohepatitis | - increased cholesterol without mallory bodies

Gastroenterology Dx (1 decks)

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