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W/Pathophysiology > Semester 2 > Flashcards

Semester 2 Flashcards

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1
Q

Genetic predisposition celiac’s

A

HLA-DQ2>HLA-DQ8

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2
Q

Autoantibodies in Celiac

A

Auto Ab vs gliadin and ETG

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3
Q

Celiac classification

A
  1. Classic
  2. Atypical
  3. Asymptomatic
  4. Latent
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4
Q

Diagnosis peptic ulcer

A

Urease breath test and biopsy

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5
Q

Diagnosis of lactose intolerance

A

Hydrogen breath test and stool pH

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6
Q

Pathogenesis model of IBD

A
  1. Environmental factors
  2. Autoimmunity
  3. Genetic factors
  4. Intestinal microbiome
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7
Q

2 major differences between ulcerative colitis and chrons

A
  1. Ulcerative colitis involves rectum

2. Ulcerative colitis has vidible bleeding while chron does not

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8
Q

Extra intestinal symptoms of U.Colitis (3)

A
  1. Anemia
  2. Arthritis
  3. Ocular lesions
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9
Q

Acute complications of ulcerative colitis

A
  1. Severe bleeding
  2. Fulminant colitis
  3. Toxic megacolon and perforation
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10
Q

Genetic factors for Chron’s

A

Modifications in JAK2 and STAT3 pathways

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11
Q

Diagnosis of Chron’s disease

A
  1. Endoscopy (cobblestone mucosa)
  2. Imaging (fistulas)
  3. Stool calprotectin and lactoferrin
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12
Q

Therapy of Chron’s disease

A
  1. Corticosteroids
  2. Vedolizumab (ab vs integrin)
  3. Anti TNF drugs
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13
Q

What is portal hypertension

A

The difference between portal vein and hepatic vein exceeds 10-12mmHg

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14
Q

What is icterus?

A

Bilirubin level is above 2-2,5 mg/dL

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15
Q

Laboratory diagnosis of liver failure

A
  1. Hepatocyte integrity : transaminases
  2. Bile secretion : bilirubin serum conc. + urine conc.
  3. Synthetic function : serum proteins + coagulation factors
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16
Q

Factors which activate stellate cells

A
  • CCL 2,7,8 : recruitement

- TGFb : activation

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17
Q

Role of stellate cells

A

Production of ECM and growth factors after liver injury

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18
Q

Diagnosis of viral hepatitis

A

HAV : serum ig
HBV : serum antigens
HCV : PCR

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19
Q

Metabolic pathologies causing liver failure

A
  1. NAFLD
  2. Haemochromatosis
  3. Alpha 1 anti trypsin deficiency
  4. Wilson’s disease
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20
Q

Mutation in Wilson’s disease

A

ATP7B protein mutation

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21
Q

Role of alpha 1 antitrypsin

A

Serin protease inhibitor

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22
Q

Enzymes of ethanol metabolism

A
  1. ADH (cytosol)
  2. CYP2E1 (ER)
  3. Catalase (peroxisome)
  4. Acetaldehyde dehydrogenase
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23
Q

Variations in ethanol metabolism

A
  1. ADH polymorphism
  2. ALDH -> ALDH2
    3 Disufiran
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24
Q

Forms of acute alcohol intoxication

A
  1. 100-300mg/dL : mild
  2. 300-400 : moderate
  3. 400-500 : severe
  4. 500 and over : death
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25
Preglomerular acute renal failure causes
- embolus - thrombotic microangiopathy - vasculitis - severe hypertension
26
Cause of IgA vasculitis
Overproduction of galactose deficient IgA
27
Primary causes of nephrotic syndrome (3)
- MCD (minimal change disease) - FSGS (focal segment glomerulosclerosis) - CNF (congenital nephrotic syndrome finnish type)
28
Symptoms of nephrotic syndrome
- edema - albuminuria - albumin deficiency - polyuria
29
Symptoms of nephritic syndrome
- edema - hematuria - oligoanuri
30
Diabetic nephropathy manifestations
- glomerulosclerosis, albumineria | - tubulointerstitial fibrosis
31
Stages of renal failure
Stage 1 : risk Stage 2 : kidney damage, GFR > 60 Stage 3 : deterioration, GFR < 60, creatinin 2-5mg/mL Stage 4 : CRF, GFR 15-30, creatinin > 5mg/mL
32
Uremic toxins based on size
Small : urea Mid : beta 2 microglobulin Big : albumin
33
Uremic toxins based on origin
Endogenous : PTH, adipokines Flora : phenols, indols, amines Exogenous : oxalate
34
Hematopoietic changes in RF
1. Normocytic anemia | 2. Thrombocytes : haematophilia
35
Bio markers of smoking induced inflammation (4)
- CRP (c-reactive protein) - IL-1B, IL-6, IL-8 - Fibrinogen (platelet aggregation) - TNFa
36
Types of smoking related inflammation in body
1. Blue bloater (cyanotic obese cardiac failure) | 2. Pink puffer (severe dyspnoe, cahexia)
37
Heart failure and copd %
20-30% have both
38
FEV1
Forced expiratory volume : volume you can push out in 1 sec
39
FVC
Forced vital capacity : volume to expire after taking in a deep breath
40
Normal and COPD FEV/FVC
Normal : 80% | COPD : less than 65%
41
Normal anion gap
12 mmol/L
42
ECG signs of right heart strain
1. ST depression and T inversion in right leads 2. Right axis deviation 3. RBBB (wide QRS) 4. S1Q3T3
43
Causes of metabolic acidosis (3)
- Increased AG : diabetic ketoacidosis, lactic acidosis | - Normal AG : renal tubular acidosis
44
Lactic acidosis value
> 2mmol/L plasma lactate
45
Hypernatremia and hyponatremia
Na > 145mmol/L | Na < 135mmol/L
46
Euvolemic hyponatremic disorder
SIADH : syndrome of inappropriate ADH
47
Rate of rehydration severe hypernatremia
10mmol/L/day
48
Renal control mechanisms for K+ (4)
1. Na/K/ATPase and NaC expression by aldosterone 2. Ça activated K+ channel 3. NCC : sodium chloride transporter (increases excretion) 4. Alpha intercalated cells : H/K/ATPase (increases reabsorption)
49
Circulatory shock
Acute systemic circulatory failure with inadequate blood supply, leading to cell and organ damage
50
Classifications of circulatory shock
1. Hypovolemic 2. Cardiogenic 3. Obstructive 4. Distributive
51
Stages of circulatory shock
1. Compensated 2. Progressive 3. Irreversible
52
Tennis staging of hypovolemic shock
1. Less than 750mL blood loss 2. 750-1500mL blood loss 3. 1500-2000mL blood loss 4. More than 2L blood loss
53
What causes irreversibility of circulatory shock (3)
1. Vicious circles (positive feedback) 2. Death of cells (necrosis) bc of metabolic changes 3. MOF
54
Effects of circulatory shock ischemia on kidney
1. Brush border damage | 2. Increase of intracellular Ca2+
55
Possible causes of cardiogenic shock
1. Myocardial infarction 2. Heart valve failure 3. Arrythmia 4. Cardiomyopathy 5. Myocarditis
56
Systemic changes in cardiogenic shock
- Systolic (decreased SV,CO) | - Diastolic (LVEDP, pulmonary congestion)
57
Treatment of cardiogenic shock
Dobutamine : increases contractility and decreases sympathetic reflex
58
Septic shock (3)
- Severe circulatory and metabolic abnormalities - requires vasopressor therapy - Plasma lactate > 2mM
59
What do PAMP and DAMP factors cause the release of in sepsis?
- NF-kb - IRF 3/7 - AP 1
60
Mechanisms of distributive shock
- Capillary leakage and edema | - systemic vasodilation (bad distribution of CO)
61
Parameters of SIRS (only need 2 for it)
- BT lover than 36 or higher than 38 - Heart rate > 90bpm - RR > 20/min - White blood cell count < 4000/µL or > 12000/µL
62
Anti inflammatory cytokines released in sepsis
- IL-10 | - TGFbeta
63
What cytokines released by effect of NF-kB
IL1, IL12, IL18
64
What is the effect of compliment activation in sepsis
- activation of plasminogen activator inhibitor | - release of TF, which activates prothrombin to thrombin
65
What is the effect of reduced thrombomodulin in spesis?
No active protein C so no inactivation of the intrinsic pathway
66
What is aging?
Progressive deterioration of physiological function associated with declining health and increased mortality
67
Syndromes that make you age fast
1. Hutchinson gilford | 2. Werner
68
What is the divison limit set by telomeres?
50
69
How many bp lost per division on telomeres?
50-100bp per division
70
How do epigenetics play a role in aging?
Increased methylation with age leads to certain gene not being expressed anymore
71
3 nutrient sensing pathways
1. mTOR 2. AMPkinase 3. Insulin/IGF1 signaling
72
Role of IGF1in cognition
- synaptic plasticity | - dendritic growth
73
How much does muscular strength decrease if immobilization?
10-20% per week
74
What is muscle atrophy
Loss of nuclei in the fiber
75
Effect of myostatin on muscle (3)
1. Inactivates PI3K pathway for protein synth 2. Inhibits myogenic genes 3. Release of ROS, causing apoptosis
76
What molecule causes osteoporosis in immobilization
Sclerostin

W/Pathophysiology (4 decks)

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