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Patho > Test 4 cases > Flashcards

Test 4 cases Flashcards

1
Q

etiology/patho of peptic ulcer disease

A

etiology: H. pylori infection
Patho: activation of immune cells including mast cells which release histamine and stimulates acid secretion contributing to the erosion/ulceration in the GI tract

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2
Q

How does the infectious agent in peptic ulcer disease trigger ulcer formations

A

Corkscrew shape which allows them to penetrate the stomach or duodenum and attach to lining
Produces urease in highly acidic environment - stimulates an increased release of gastrin

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3
Q

Dx of peptic ulcer disease

A

guaiac test, urea breath test

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4
Q

Tx peptic ulcer disease

A

antibiotics, PPIs (omeprazole)

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5
Q

what is the greatest predictor of crohn’s disease?

A

family hx

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6
Q

What population has an increased risk for developing crohn’s disease?

A

smokers - two-fold risk

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7
Q

Patho of crohns

A

chronic inflammatory disease of the GI tract that extends through the intestinal wall form mucosa to serosa.
Any part of the GI tract can be afcected

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8
Q

What are two unique features that are present in crohn’s but not ulcerative colitis?

A

skip lesions and cobblestone appearance

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9
Q

What genes are affected in celiac disease?

A

HLA class 2 genes DQ2 and DQ8

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10
Q

Patho of celiac disease

A

inappropriate t-cell mediated response against alpha-gliadin (a component in gluten)

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11
Q

Dx and tx of celiac

A

dx: serology for antibodies, genetic testing
tx: gluten free diet

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12
Q

How long can it take for a celiac patient to see effects of a gluten-free diet?

A

2-18 months

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13
Q

Patho of liver cirrhosis

A

Liver tissue replaced by fibrosis, scar tissue and regenerative nodules - loss of liver function

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14
Q

How does liver cirrhosis lead to issues with clotting factors?

A

Decreased production of bile which leads to decreased fat and Vit K absorption; decreased production of prothrombin

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15
Q

Patho behind major complications of cirrhosis: portal hypertension, steatorrhea, hepatic encephalopathy, jaundice, ascites, edema

A

Portal hypertension occurs when blood flow through liver is impaired due to cirrhosis

Steatorrhea: Impaired synthesis and secretion of bile - impaired fat absorption

Hepatic encephalopathy: Impaired amino acid interconversion - increased levels of ammonia, fibrosis, blood diversion from hepatic circulation

Jaundice: buildup of bilirubin in the blood stream

Ascites: increased hydrostatic pressure due to portal hypertension

Edema: decreased capillary colloidal osmotic pressure due to decreased albumin production

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16
Q

What are the major causes of acute pancreatitis?

A

Short term alcohol overuse, gallstones, pancreatic cancer

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17
Q

Patho behind acute pancreatitis

A

Reversible inflammatory process of pancreatic acini, premature activation of pancreatic enzymes due to blockage of bile duct or alcohol

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18
Q

Complications of acute pancreatitis

A

necrosis leading to organ failure, high mortality rate 20-30%

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19
Q

What is the main diagnostic test for acute pancreatitis?

A

Serum amylase or lipase

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20
Q

Patho of myasthenia gravis

A

antibodies reduce or block excitation-contraction coupling at the NMJ, compromises ability of skeletal muscle to contract and maintain contraction

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21
Q

What phenomena does not occur in myasthenia gravis

A

summation - occurrence of additional twitch contractions before the previous twitch has completely relaxed

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22
Q

Dx of myasthenia gravis

A

repetitive electromyography - with more stimulation, will have weaker contractions

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23
Q

Tx of myasthenia gravis

A

anticholinesterase inhibitor, immunosuppressants

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24
Q

Define open vs. closed fracture

A

• Open fracture: bone protruding through skin

Closed fracture: no skin

25
Q

What is a complication of fracture, and what is the infectious agent?

A

osteomyelitis

staph aureus

26
Q

How do fat emboli occur with fracture?

A

fat globules released and attract platelets which create microemboli and occlude small blood vessels

27
Q

Risk factors for osteoporosis

A

advanced age
women
smoking

28
Q

patho of osteoporosis

A

bone loss exceeds bone growth

29
Q

how is osteoporosis linked to decreasing estrogen values?

A

decreasing estrogen = increased osteoclasts

30
Q

How does osteoporosis usually present?

A

multiple fractures

31
Q

Tx osteoporosis

A

estrogen replacement, biphosphonates

32
Q

Risk factors for paget’s

A

family history

occurs mostly in north america, australia, NZ

33
Q

Patho of paget’s

A

accelerated pattern of bone remodeling - rapid bone breakdown followed by short periods of bone formation

34
Q

Sx of pagets

A

bone pain, fractures

35
Q

What is the main diagnostic for paget’s and what diseases does it rule out?

A

elevated serum alkaline phosphatase

not seen in osteoporosis or osteoarthritis

36
Q

What are the normal functions of skin that are affected by burns?

A

infection prevention
temp regulation
fluid retention
sensory

37
Q

What layers are affected in first-degree/superficial burns?

A

outer layers of the epidermis only

38
Q

What layers are affected in second-degree partial thickness vs. deep dermal partial thickness burns?

A

partial: epidermis and part of the dermis

deep dermal: epidermis and entire or most of dermis

39
Q

Deep dermal partial thickness - what function is lost and how long does it take to recover?

A

Sensory

weeks

40
Q

What layers are affected in third-degree/full thickness burns? What is most affected, how long does it take to heal and what does the skin look like?

A

epidermis, dermis, subcutaneous tissue, may involve muscle and bone

capillaries, veins and nerves destroyed
months to heal
red, white, black or leathery skin

41
Q

What is used to determine the extent of injury in skin burns

A

Rule of nines

42
Q

Complications of skin burns (9)

A
  1. Renal failure
  2. myoglobinuria, 3. hemoglobinuria
  3. multi-organ failure
  4. Hypovolemic shock
  5. infections
  6. Edema
  7. Desiccation = removal of water from blood vessels
  8. Electrolyte imbalances
43
Q

Tx of burns

A

fluid replacement

ventilation support

44
Q

ALL: risk factors, genetic changes

Prevalence of cases with genetic changes

A

Risk factors genetics
Changes: numeric and structural changes in chromosomes of leukemic cells
90% of cases

45
Q

Dx of ALL

A

cytogenic studies to determine chromosomal abnormalities

46
Q

Patho of ALL

A

Lymphoid precursors proliferate and replace normal hematopoietic cells of the marrow – typically affects B cells rather than T

47
Q

What are the two main causes of DIC?

A

OB disorders: tissue factors released from necrotic placental or fetal tissue

infection/trauma: endothelial cell injury through intrinsic or extrinsic pathway

48
Q

Patho of DIC

A

Consumptive disorder that initiates overwhelming clotting in response to an event where clotting factors and platelets are consumed

49
Q

Define thrombocytopenia

A

thrombin induced platelet aggregation reduces circulating platelets

50
Q

What does PT measure

A

evaluates how long it takes for a clot to form in a blood sample

51
Q

What does aPTT measure

A

evaluates coagulation factors prekallikrein and kininogen

52
Q

RA: what is a pannus?

A

synovial sac becomes thick and covered in granular tissue, can spread through tissue and cause scarring

53
Q

Tx of RA

A

NSAIDs, corticosteroids

54
Q

What do 85% of cases of atopic dermatitis have in common

A

personal or family history of allergic rhinitis or asthma

55
Q

Patho of atopic dermatitis

A

Relapsing inflammatory skin condition, associated with asthma or hay fever to be defined as atopic dermatitis

56
Q

Phases of wound healing (3)

A

Inflammatory phase: hemostasis and phagocytes clean site

Proliferative phase: collagen helps build new tissue, formation of granulation tissue occurs during this phase – highly vascular CT that forms

Remodeling phase: fibrous scar becomes smaller and stronger

57
Q

Define resolution, regeneration, replacement

A

resolution: minimal tissue damage that is fully restored
regeneration: cells are replaced by proliferation of similar nearby cells, normal structure and function at the area of injury
replacement: extensive damage, cells cannot complete mitosis, fibrous tissue and scar formation

58
Q

Define first intention vs. second intention healing

A

First: scar tissue laid across a clean wound with edges in close approximation

Second: occurs in wounds in which large sections of tissue have been lost or in wounds complicated by infection

59
Q

Factors of compromised wound healing (4)

A
  1. impaired blood flow and O2 delivery
  2. impaired inflammatory and immune response
  3. malnutrition
  4. medications

Patho (14 decks)

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