Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Patho > Test 4 cases > Flashcards

Test 4 cases Flashcards

(59 cards)

Start Studying
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

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

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

Dx of peptic ulcer disease

A

guaiac test, urea breath test

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

Tx peptic ulcer disease

A

antibiotics, PPIs (omeprazole)

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

what is the greatest predictor of crohn’s disease?

A

family hx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

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

A

smokers - two-fold risk

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

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

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

A

skip lesions and cobblestone appearance

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

What genes are affected in celiac disease?

A

HLA class 2 genes DQ2 and DQ8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Patho of celiac disease

A

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

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

Dx and tx of celiac

A

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

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

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

A

2-18 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Patho of liver cirrhosis

A

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

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

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

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

What are the major causes of acute pancreatitis?

A

Short term alcohol overuse, gallstones, pancreatic cancer

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

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

Complications of acute pancreatitis

A

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

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

What is the main diagnostic test for acute pancreatitis?

A

Serum amylase or lipase

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

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

What phenomena does not occur in myasthenia gravis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Dx of myasthenia gravis

A

repetitive electromyography - with more stimulation, will have weaker contractions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Tx of myasthenia gravis

A

anticholinesterase inhibitor, immunosuppressants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Define open vs. closed fracture

Study These Flashcards
A

• Open fracture: bone protruding through skin

Closed fracture: no skin

25
What is a complication of fracture, and what is the infectious agent?
osteomyelitis | staph aureus
26
How do fat emboli occur with fracture?
fat globules released and attract platelets which create microemboli and occlude small blood vessels
27
Risk factors for osteoporosis
advanced age women smoking
28
patho of osteoporosis
bone loss exceeds bone growth
29
how is osteoporosis linked to decreasing estrogen values?
decreasing estrogen = increased osteoclasts
30
How does osteoporosis usually present?
multiple fractures
31
Tx osteoporosis
estrogen replacement, biphosphonates
32
Risk factors for paget's
family history | occurs mostly in north america, australia, NZ
33
Patho of paget's
accelerated pattern of bone remodeling - rapid bone breakdown followed by short periods of bone formation
34
Sx of pagets
bone pain, fractures
35
What is the main diagnostic for paget's and what diseases does it rule out?
elevated serum alkaline phosphatase | not seen in osteoporosis or osteoarthritis
36
What are the normal functions of skin that are affected by burns?
infection prevention temp regulation fluid retention sensory
37
What layers are affected in first-degree/superficial burns?
outer layers of the epidermis only
38
What layers are affected in second-degree partial thickness vs. deep dermal partial thickness burns?
partial: epidermis and part of the dermis | deep dermal: epidermis and entire or most of dermis
39
Deep dermal partial thickness - what function is lost and how long does it take to recover?
Sensory | weeks
40
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?
epidermis, dermis, subcutaneous tissue, may involve muscle and bone capillaries, veins and nerves destroyed months to heal red, white, black or leathery skin
41
What is used to determine the extent of injury in skin burns
Rule of nines
42
Complications of skin burns (9)
1. Renal failure 2. myoglobinuria, 3. hemoglobinuria 4. multi-organ failure 5. Hypovolemic shock 6. infections 7. Edema 8. Desiccation = removal of water from blood vessels 9. Electrolyte imbalances
43
Tx of burns
fluid replacement | ventilation support
44
ALL: risk factors, genetic changes | Prevalence of cases with genetic changes
Risk factors genetics Changes: numeric and structural changes in chromosomes of leukemic cells 90% of cases
45
Dx of ALL
cytogenic studies to determine chromosomal abnormalities
46
Patho of ALL
Lymphoid precursors proliferate and replace normal hematopoietic cells of the marrow – typically affects B cells rather than T
47
What are the two main causes of DIC?
OB disorders: tissue factors released from necrotic placental or fetal tissue infection/trauma: endothelial cell injury through intrinsic or extrinsic pathway
48
Patho of DIC
Consumptive disorder that initiates overwhelming clotting in response to an event where clotting factors and platelets are consumed
49
Define thrombocytopenia
thrombin induced platelet aggregation reduces circulating platelets
50
What does PT measure
evaluates how long it takes for a clot to form in a blood sample
51
What does aPTT measure
evaluates coagulation factors prekallikrein and kininogen
52
RA: what is a pannus?
synovial sac becomes thick and covered in granular tissue, can spread through tissue and cause scarring
53
Tx of RA
NSAIDs, corticosteroids
54
What do 85% of cases of atopic dermatitis have in common
personal or family history of allergic rhinitis or asthma
55
Patho of atopic dermatitis
Relapsing inflammatory skin condition, associated with asthma or hay fever to be defined as atopic dermatitis
56
Phases of wound healing (3)
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
Define resolution, regeneration, replacement
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
Define first intention vs. second intention healing
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
Factors of compromised wound healing (4)
1. impaired blood flow and O2 delivery 2. impaired inflammatory and immune response 3. malnutrition 4. medications

Patho (14 decks)

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