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Phase 2a > Pathology/ immunology/ pharmacology > Flashcards

Pathology/ immunology/ pharmacology Flashcards

1
Q

Why are clots rare?

A
  • laminar flow
  • endothelial cells arent sticky when healthy
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2
Q

positive feedback loops in clot formation?

A
  • platelet release chemicals when they aggregate
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3
Q

thrombosis definition

A

is the formation of a solid mass from blood constituents in
an intact vessel in a living person.

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4
Q

3 things to cause thrombosis?

A
  • change in laminar flow
  • change in blood constituents (too many platelets)
  • change in vessel wall
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5
Q

What can damage endothelial cells?

A
  • nicotine
    damages vessel wall and ruins blood flow because of damaged wall
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6
Q

embolism def?

A

solid mass in the blood being carried
through the circulation to a place where it gets stuck and
blocks the vessel.

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7
Q

virchows triad?

A

3 factors creating a thrombosis
- change in laminar flow
- change in blood constituents (too many platelets)
- change in vessel wall

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8
Q

commonest cause of embolus?

A

deep vein thrombosis

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9
Q

example of common sites of an embolus?

A

mural thrombus overlying a myocardial infarct
in the left ventricle can go anywhere is the systemic
circulation

cholesterol crystals from an atheromatous plaque
in the descending aorta

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10
Q

emboli travels in venous system where does it travel ?

A

right side of heart via vena cava into the pulmonary arteries - cant go further because lungs go down to capillary size

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11
Q

emboli travels in arterial system where does it travel ?

A

can travel anywhere downstream

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12
Q

why do get redness/heat during inflammation?

A

vasodilation/ increased blood flow

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13
Q

why do you get swelling during inflammation?

A

oedma
physical cell mass

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14
Q

how long do neutrophils live?

A

short life span

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15
Q

how long do macrophages live?

A

long life span of weeks to months

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16
Q

how does histamine increase blood flow ?

A

open pre capillary sphinctors

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17
Q

what prevents endothelial cells from sticking?

A

release of NO

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18
Q

what produces prostaglandin?

A

prostaglandin synthase

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19
Q

how long to lymphocytes live?

A

years

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20
Q

how does oedma occur in acute inflammation?

A

excess fluid leaks out of capillaries into tissues along with plasma proteins

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21
Q

roles of fibroblasts?

A

produce collagen in areas of chronic inflammation and repair

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22
Q

what is TB ?

A

mycobacteria ingested by macrophages however can not kill the mycobacteria
fibrosis occurs

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23
Q

what is a granuloma ?

A

A granuloma is a collection of immune cells and a type of chronic inflammation. Granulomas are made up of specialized immune cells including lymphocytes, histiocytes, and multi-nucleated giant cells
feature of some chronic inflammation conditions

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24
Q

conditions where granuloma is found?

A

TB, leprosy, chrons disease

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25
Q

second intention healing?

A

loss of tissue and repairs involve granulation tissue
white scar with collagen left over

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26
Q

main lipid in atheroscolsis?

A

cholesterol

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27
Q

preventing platelet aggregation?

A

low dose aspirin a day

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28
Q

How does atherosclerosis form?

A

fatty streak
accumulated endothelial damage - LDL
primary platelet plug
fibrous cap
thrombosis forms and then heals on top
Thrombosis keeps forming on top of atherosclerosis clots

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29
Q

complications of atherosclerosis?

A

aortic aneurysm

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30
Q

Why do cells apoptosis?

A

DNA damage

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31
Q

Cancer and apoptosis?

A

lack of apoptosis in cancer

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32
Q

what happens during pancreatitis?

A

Pancreas become inflamed and eats its self
form of necrosis

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33
Q

what do intrinsic apoptotic factors respond to?

A

growth factor deprivation and biochemical stress such as DNA damage from UV rays

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34
Q

BCL 2 role in apoptosis?

A

inhibits factors that induce apoptosis - part of intrinsic apoptosis

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35
Q

BAX role in apoptosis?

A

factors enhancing apoptosis - Part of the intrinsic apoptosis

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36
Q

Extrinsic apoptosis?
receptors ?

A

The specific mechanism for the activation of apoptosis characterised by
ligand-binding at death receptors on the cell surface
TNFR 1
FAS

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37
Q

results of extrinsic and intrinsic apoptosis?

A

cascade the activation of caspases

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38
Q

inhibitors of apoptosis?

A

growth factors
extracellular cell matrix
sex steroids

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39
Q

the neurotransmitter of chloergeneric pharmacology?

A

acetylcholine

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40
Q

tissue in hypertrophy example

A

occurs in organs where cells cannot divide
* examples - skeletal muscle in athletes/bodybuilders

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41
Q

tissue in hyperplasia example

A

occurs in organs where cells can divide
* examples - benign prostatic hyperplasia, endometrial
hyperplasia

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42
Q

tissue in mixed hyperplasia/ hypertrophy example

A

occurs in organs where cells can divide
* example - smooth muscle cells of the uterus during
pregnancy

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43
Q

atrophy examples

A

Alzheimer’s dementia, quadriceps muscle
following knee injuries

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44
Q

dysplasia examples

A

bronchial epithelium in cigarette smokers:
metaplasia from ciliated to squamous epithelium, then
development of dysplasia in the squamous epithelium

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45
Q

causes of dysplasia

A

longstanding irritation, chronic inflammation, or certain carcinogenic substances

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46
Q

polygenic diseases example?

A

Breast cancer risk is an example There are some genes, such as BRCA1 and BRCA2, which do have a large individual effect but most of breast cancer risk is composed of incremental rises in risks by tens to hundreds of apparently unrelated genes even when there is strong family histor

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47
Q

congenital disease?

A

disease someone is born with
may be genetic or acquired in the development

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48
Q

Atherogenesis steps?

A
  1. endothelial cell wall damage
  2. LDL accumulates in the arterial wall
  3. macrophages accumulate at the site of damage and cause inflammation
  4. formation of fatty streak
  5. smooth muscles increases around ldl core and fibrous cap forms
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49
Q

role of monocytes in acute inflammation?

A

migrate to tissues and become macrophages and secrete chemical mediators for chemotaxis

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50
Q

most common tumour spread?

A

tumours that grow locally and then naturally move around the body. eg: breast cancer and colorectal cancer

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51
Q

spread of basal cell carcinoma?

A

only spread locally and do not spread (metastasise) to other parts of the body

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52
Q

spread of leukaemia?

A

arise from cells that naturally move around the body

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53
Q

sarcoma?

A

tumour growing in connective tissue

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54
Q

oncogenesis?

A

formation of benign and malignant tumours from normal tissue

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55
Q

tumour ?

A

abnormal swelling

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56
Q

why can neoplasm not arise in erythrocytes?

A

erythrocytes don’t have nuclei

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57
Q

HPV linked to which cancer

A

cervical cancer

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58
Q

extravasation?

A

increased leukocyte transendothelial migration is also known diapedesis

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59
Q

where do all leukocytes originate from?

A

hematopoietic stem cells in red blood marrow

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60
Q

lymphocytes?

A

B cell, T cell and large granular lymphocyte

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61
Q

role of basophils?

A

release IL-4 (promotes IgE production) and histamine

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62
Q

presence of eosinophils and granulomas?

A

parasitic infection

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63
Q

role of eosinophils?

A

cause production of prostaglandins and cytokines and releases granular proteins

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64
Q

What is the name of the main effector cell in
acute inflammation?

A

neutrophil polymorphs

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65
Q

What is the name of the cells that produce
collagen in fibrous scarring?

A

fibroblasts

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66
Q

where are most of the cancer risks from?

A

85% environmental - latent internal may be decades

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67
Q

oesophageal cancer risks?

A

Japan, Chine - diet
turkey, Iran - scalding hot drinks burns the throat

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68
Q

Asbestos cancer risks?

A

bladder cancer and mesothelioma

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69
Q

chemical carcinogens how do they do this?

A

must be metabolised from pro-carcinogens to ultimate carcinogens

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70
Q

classifications of viral carcinogens?

A

DNA virus or RNA virus

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71
Q

UV rays or suncream which according to evidence could cause skin cancer?

A

UV rays

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72
Q

Which one of the following does
granulomatous inflammation occur?
A. Crohn’s disease
B. Acute appendicitis
C. Infectious
mononucleosis
D. Lobar pneumonia

A

A chrons disease

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73
Q

inherited predispositions for developing cancer examples?

A

colonic polyps
ulcerative colitis
cervical dysplasia

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74
Q

Which one of the following is chronic inflammation from the start:
appendicitis
cholecystitis
infectious mononucleosis

A

infectious mononucleosis
“mono” “gladular fever”
enlargement of spleen

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75
Q

why fever during inflammation?

A

macrophages and polymorphs release endogenous pyrogens (IL-6, IL- 1, TNF) acting on the hypothalamus to set thermoregulatory mechanisms at a higher temp

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76
Q

what endogenous pyrogens respond to?

A

exogenous pyrogen (virus, bacteria)
chemical agents

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77
Q

what is the differentiation pattern of metaplastic cells lining cigarette smokers’ bronchi?

A

ciliated with mucociliary escalator to squamous epithelium

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78
Q

Gram positive patterns?

A

thick cell wall, no outer envelope

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79
Q

gram negative patterns?

A

thinner cell with outer envelope

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80
Q

what does TLR 1/2 DETECT?

A

GRAM positive bacteria
lipoproteins

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81
Q

what does tlr 4 detect?

A

lipopolysaccharides of gram-positive bacteria

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82
Q

which tlr detects flagella ?

A

TLR 5

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82
Q

which tlr detects flagella ?

A

TLR 5

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83
Q

which tlr are within the endosome?

A

tlr 3, tlr 7, tlr 9 , tlr 8

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84
Q

tlr 7 detects ?

A

single stranded ran

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85
Q

complement system activation pathways?

A

classical - antibody antigen
alternative - bacteria endotoxins
lectin - Manose binding protein

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86
Q

describe opsonisation.

A

caused by c3 b activation and triggers phagocytosis

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87
Q

In situ carcinoma?

A

carcinoma within collagen basement membrane not spreading

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88
Q

invasive carcinoma?

A

carcinoma through the collagen basement membrane and arrives into the extracellular matrix could reach blood vessels or lymphatic

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89
Q

where are tlr found?

A

macrophages, dendritic cells and neutrophils

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90
Q

which important surface receptors do dendritic cells have?

A

tlr and mhc 2

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91
Q

describe the process of active immunity.

A

vaccine
- engage innate immune system (dendritic cells, neutrophils
- danger signals (PAMPs, TLR release of cytokines and proinflammatory)
- activate antigen-presenting cells (Langerhans cells)
- engage the adaptive immune system and memory in t cells and b cells

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92
Q

5 immunoglobulins classes?

A

GAMED
IgG
IgM
IgA
IgE
IgD

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93
Q

HOW DO THE iG classes differ?

A

different heavy chain structure

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94
Q

Ig involved in parasitic infections?

A

IgE

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95
Q

effect of fab in antibodies role?

A
  • neutralize toxins
  • prevent binding
  • form complexes
  • immobilizes motile microbes
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96
Q

role of fc receptors in antibdies ?

A
  • trigers phagocytes
  • nk cells - enhanced killed of infected cells
  • mast cells - releases inflammatory mediators (tnf alpha + histamine)
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97
Q

role of cytokines?

A

control behaviour of leukocytes (nuetrophil, monocytes - macrophages, basophils)

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98
Q

what antigens do t cells recognize?

A

cell-associated not free soluble antigens

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99
Q

role of mhc?

A

initate t cell response

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100
Q

which t cell does mhc1 present too?

A

CD8+ (CYTOTOXIC)

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101
Q

WHICH t cell does mhc 2 present too?

A

cd4+ helper

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102
Q

role of TH2?

A

TRIGGER B CELLS to release ige and promote release of inflammatory mediators

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103
Q

role of afferent lymphatic vessels?

A

carries dendritic cells with bacterium from the site of infection to naive t cells
dendritic cells activate t cells
- trigger plasma cells to release antibodies
- create effector t cells

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104
Q

cells from common myeloid progenitor ?

A
  • eosinophil
    nutrophil
    basophils
    mast cells
    monocyte - macrophage
    dendritic cells
    megakryocyte
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105
Q

cells from common lymphoid progenitor?

A

t cells
b cells
natural killer cell

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106
Q

THC 1 triggers which ig release?

A

b cells to relase IGg (main class in serum and tissues)

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107
Q

THC 2 triggers which ig release?

A

b cells to release ige to release inflammatory mediators such as histamine and tnf alpha

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108
Q

mechanism of statins?

A

stops the liver from producing cholesterol

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109
Q

4 a FOR TREATING cardiovascular disease

A

aspirin
statin
beta blockers
ace inhibitors

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110
Q

2 types of cholinergic receptors?

A

muscaneric (parasympathetic) and nicotinic

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111
Q

types of muscarinic receptors? and what do they effect?

A

M1 - Mainly in the brain
M2- mainly in the heart slows down
M3- Glandular and smooth muscle
bronchoconstriction
sweating
salivary gland secretion
M4 + M5 - CNS

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112
Q

M2 on SA and AV node?

A

SA - decreases HR
AV - induce av node block increases PR interval

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113
Q

pre ganglionic receptors? and neurotransmitter?

A

receptor - nicotinic
neurotransmitter - ACh
both para and sympathetic

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114
Q

post ganglionic
receptors?
neurotransmitters?

A

parasympathetic
muscarinic + ACh

sympathetic
alpha/ beta receptors + noradrenaline

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115
Q

skeletal muscle (voluntary) uses which receptors to contract?

A

nicotinic receptors

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116
Q

cholinergic crisis?

A

excessive stimulation of ACh on nicotinic receptors
parasympathetic nervous system in overdrive

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117
Q

cholinergic crisis sludge?

A

symptoms of crisis:
S - salivation
L - LACRIMATION tears
U - URINATION
D - DEFEACATION
G- gi UPSET CRAMPING VOMITING
E - vomiting

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118
Q

receptor in the somatic nervous system? neurotransmitters?

A

nicotinic receptors (n1)
ACh

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119
Q

how do LDL and HDL increase plaque formation?

A

increases the number of foam cells to build plaque

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120
Q

what are foam cells?

A

These are macrophages that have phagocytosed oxidised lipoproteins -
they have large amounts of cytoplasm with a foamy appearance

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121
Q

structural differences in the somatic and autonomic nervous systems?

A

somatic - single nurone from CNS to muscle
autonomic - there are two nerves in series,
the pre- and post-ganglionic fibres.

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122
Q

what is the name of a maligant tumour of straiated muscle? ?

A

rhabdo myo sarcoma
sarcoma - tumour in connective tissue

123
Q

cancer of epithlium ?

A

carcinoma

124
Q

adenoma?

A

a benign tumour in glandular tissue - very common

125
Q

screening for breast cancer screening?

A

mammogram

126
Q

screenign for coloractal cancer?

A

FIT test - testing for blood in faeces

127
Q

cervical cancer screening?

A

smear test

128
Q

how to detect lung cancer?

A

ct scans

129
Q

name some carcinogens?

A

hepatitis c
aromatic amines
ionising radiation
aflatoxin - hepatocellular carcinoma

130
Q

adenocarcinoma?

A

malignant tumour in glandular tissue

131
Q

what is a receptor?

A

compenent of a cell that interact with a ligand and intiates and a biochemical change

132
Q

exmaple of irreversible antagonist ?

A

BAAM

133
Q

two types of inhibitors ?

A

irreversible inhibitors
reversible inhibitors bind non covalently

134
Q

active transporters examples?

A

ATPase required
moves aginst ions gradient

135
Q

types of protein ports?

A

uniport
symporters
co transporters

136
Q

where are ions channels found?

A

most tissues
epithial sodium channel
voltage gated (calcium, sodium)
metabolic (potassium)
receptor activated (chloride)

137
Q

Where are epithelial sodium channels sound?

A

found in kindeys and GI
reabsoprtoion of na+ at collecting ducts

138
Q

ROLE AMLODIPINE ?

A

angioselective
on smooth muscle cell by inhibiting
vasodilation - lowers bp
inhibits Ca influx across cell membranes

139
Q

3 states of voltage-gated sodium and potassium channels

A

closed
open
inactive

140
Q

role of voltage gated potassium channels ?

A

regulates insulin secretion from pancreas
increased glucose leads to block of ATP dependant K+ channels
reptitice firing of action potentials increases Ca+ influx and triggers insulin secretion

141
Q

do receptor mediated chloride channels have mulitble binding sites?

A

yes

142
Q

antiporter activity

A

moves ions against their conc gradients

143
Q

sodium (na/k atapase ) pump how much pumped in and out?

A

3 Na - to extracellular (out)
2 k - intracellular (in)

144
Q

type of inhibition in omeprazole?

A

irreversible inhibitors
inhibits h/k ATPase (ppi)

145
Q

Pharmacokietics

A

study of drug metabolism

146
Q

pharmacokinetics ADME?

A

Absorption - how will it get in?
metabolism - how is it broken down? liver?
distribution - where will it go?
excretion - how does it leave?

147
Q

where are human CYPS located?
role

A

inner membrane of mitochondria
the endoplasmic reticulum of cells
75% of total metabolism - deactivates or activates drugs

148
Q

What are the two types of immune response in humans?

A

innate and acquired

149
Q

Which of the following are features of the adaptive immune response?

Does not require prior contact with the pathogen

It works with B and T lymphocytes

Lacks specificity

Lectin type molecules

Unmethylated CpG sequences

A

unmethylated cpg sequences
lectin type molecules

150
Q

which immune response are PRR molecules part of?

A

innate

151
Q

role of MBL (mannose binding lectin) ?

A

is a PRR of innate immune system
recognises PAMPs
activates the complement system

152
Q

Polysaccharide vaccines are composed of long chains of sugar molecules that make up the surface capsule of certain bacteria. These vaccines are available for the treatment of which of the following diseases?

Pneumococcal disease

Influenza type b

Rabies

Salmonella Typhi

Meningococcal diseas

A

pnuemococcal
salmonella
meningococcal

153
Q

chemoattraction of leukocytes and phagocytosis are…

A

forms of PRR

154
Q

what is catalase test?

A
155
Q

what causes endocarditis ?

A
156
Q

mycobactiera stian? examples

A

TB
zhiel neelsen stain

157
Q

come in and stain?

A
158
Q

MRSA ?

A

RESITTED STRAIN OF staphycocci aureus

159
Q

why of infectioin of s epidermidis?

A

infections are opportunisitc
- attacks immune comprised patienst

160
Q

how does antigenic sero grouping work?

A
161
Q

role of streptokinase ?

A

spreading streptokinase
breaks down clots
C5a peptidase
- reduces chemotaxis

162
Q

For which group of bacteria should you do an optochin test?
A: identifies staph aureus
B: identifies staph from non-staph
C: identifies mycobacterium
D: identifies fungi

A

staph from non staph

163
Q

role of c tentani?

A

tetanus is gram anaerobic positive bacilli
inhibits GABA and causes muscle contractions

164
Q

rash during anaphylaxis ?

A

direct response to histamines
fluid leaking out of dermis - angioedema

165
Q

type 1 hypersensitivity sensation stage?

A

initial exposure to allergen
antigen brought to lymph nodes
In allergy: antigen-presenting cells also present costimulating molecules
The body releases IgE and attach to mast cells
no further response

166
Q

second exposure type 1 hypersensitivity stage?

A

Second exposure
Encounters allergen again and IgE are already made and primed with mast cells
Allergen binds to IgE-primed mast cells and mast cells degenerate and histamine is released with pro-inflammatory mediators

167
Q

Adrenaline role in anaphylaixs ?

A

suppress histamine release
restores cardiac output

168
Q

role of autonomic nervous system?

A

Conveys ALL outputs from CNS to the body except voluntary stuff

169
Q

adrenergic ?

A

relating to (nor)adrenaline and their receptors

170
Q

location of sympathetic preganglionic nerve?

A

lateral horn of the spinal cord (T1- L2)

171
Q

Sacral location of parasympathetic nerves?

A

T12/L1 outflow in S2-S4

172
Q

NORADRENLINE ACTS ON WHICH RECEPTORS ? which ganglion? which autonomic system?

A

beta and alpha receptors (smooth + cardiac muscle)
post ganglion
sympathetic

173
Q

neurotransmitter for sweat glands?

A

sympathetic post-ganglionic fibres release
acetylcholine to stimulate muscarinic receptors
this is an exception

174
Q

neurotransmitter for somatic nervous system?

A

ACh

175
Q

where is noradrenline released?

A

released from sympathetic nerve fibre ends

176
Q

where is adrenline rleeased?

A

adrenal glands

177
Q

alpha 1 agonism? nuerotransmitter?

A

Alpha 1 agonism causes vasoconstriction, mainly in the skin and splanchic
(abdominal) beds
noradrenaline

178
Q

alpha 1 antagonist ?

A

doxazosin (generally less frequently used
than modern antihypertensive)
lowers bp

179
Q

where are beta 1 receptors found?

A

◦ Heart
◦ Kidney
◦ Fat cells

180
Q

beta 1 agonism leads to ? neurotransmitters?

A

Tachycardia
◦ Increase in stroke volume
◦ Renin release (increase in vascular tone)
◦ Lipolysis and hyperglycaemia
Noradrenline + adrenline

181
Q

beta 2 receptors location?

A

bronchi - bronchodilation
bl;adder wall - inhibits micturation
uterus - inhibition of labour
skeltal muslce - increase contraction speed
pancreas - insulin and glucagon secretion

182
Q

beta 2 agonist drugs?

A

Agonist drugs (e.g. salbutamol) are very useful in asthma and
chronic obstructive pulmonary disease

Side effects include tremor hyperglycaemia (glucagon release) and
tachyarrythmia

183
Q

how long does morphine last ?

A

3-4 hours

184
Q

potency 0f diamorphine?

A

binding affinity
5mg
passes through blood brain barrier quicker

185
Q

why do not all drugs make it into circulation?

A

first pass metabolism
gut and liver metabolise before getting into circulation

186
Q

how much of the population is absent of cyp2d6?

A

10%

187
Q

examples of drugs that require cyp2d6 to be metabolsied?

A

tramadol - needs to be metabolised by CYP2D6 to o-desmethyl
tramadol to be active
codine

188
Q

levels of hypersensity represent what?

A

Type 1 and 2 are IG responses
Type 3 and type 4 are cell mediated
Further down is about how much the body responds

189
Q

sensation phase in allergy?

A

T cell bring antigen to lympnodes
In allergy antigen-presenting cells also present costimulating molecules
Then body releases IgE and attach to mast cells

190
Q

second exposure phase in allergy?

A

Encounters allergen again and IgE are already made and primed with mast cells
Allergen binds to ige primed mast cells and mast cells degenerate and histamine is released with proinflammatory mediators

191
Q

late phase in allergy?

A

Proinflammatory mediates stimulates of basophils

192
Q

blood test for anaphylaxis ?

A

tryptase levels which are elevated 3 hours after anaphylaxis
secreted by mast cells

193
Q

prevalence?

A

probabilty of having disease at a given time point

194
Q

incidence?

A

probabilty of getting disease during a specified time period

195
Q

effects of adrenline on alpha 1 , beta 1 and beta 2 receptors?

A

Alpha 1- adrenoreceptors : increases BP + coronary perfusion
Beta 1 - adrenoreceptors: positive ionotrophic (heart rate contracts stronger) + positive chronotropic (increase HR)
Beta2 - adrenoreceptors: reduces oedma and bronchocontrcition
Reduces release of inflammatory mediators by increase cAMP in mast cells and basophils

196
Q

risk factors for ADRS

A

F>M
elderly
neonates
polypharmacy
atopy

197
Q

how does aspirin work?

A

LOW DOSES inhibits COX 1
HIGH DOSES INHIBITS cox 1 and 2

198
Q

role of cox 1and 2?

A

cox 1 - produces thromboxane ]causes vasoconstriction and platelet agreggeation
cox 2 - produces prostaglandins and causes inflammation and pain

199
Q

most common drugs to have ADRS?

A

ANTIBITOICS
ANTINEOPLASTICS - cancer treatment
cardiovascular drugs
NSAIDS
cns DRUGS

200
Q

tellow card scheme ?

A

voluntary ADR reporting scheme - reports to MHRA
ALL SUSPECTED REACTIONS - HERBAL MEDICINES OR DRUGS

201
Q

type 2 reactions example?

A

methyl-dopa-induced haemolytic anaemia
drug induced haemolysis

202
Q

type 3 reactions examples ?

A

glomerulonenephritis

203
Q

type 4 reactions example?

A

contact dermatitis -eczema
steven johnson syndrome

204
Q

how does paracetmol overdose cocur?
cure?

A

uses up glutathione stores (makes paracemol a stable metabolite) - builds up dangerous metabolise - cellular necorissi
activated charcoal - glutathione trasferase reverses reaction

205
Q

role of enalalrpil ?

A

ace inhibitpr to treat hypertension and heart failure
no ace 2
and bradykinin remains as vasodilator

206
Q

contraindication of enalapril in what condition?
most common side effect
not prescribed for patented with egfr of less than?

A

renal artery stenosis
dry cough
60

207
Q

factors that influence the activity of an antagonist are?

A

affinity of antagonist for the receptor

208
Q

what happens when B2 adrenoreceptors is stimulated?

A

bronchodilation

209
Q

irreversibile enzyme inhibitor?

A

aspirin

210
Q

5 catagories of protozoa ?

A

flagellates
Amoebae
Sporozoans
Ciliates
- Microsporidia:

211
Q

tests for malaria?

A

blood film Plasmodium ovale trophozite! posotive

212
Q

mycotoxins

A

toxins released by fungi

213
Q

t cell deficiency (HIV) increases susceptibility to?

A

fungi - yeast (candida spp)
virus - herpes
MALIGENCIES (EPSTEIN BARR VIRUS)
autimmune viruses

214
Q

what are catalase positive

A

gram neagtive bacteria - e coli
fungi

215
Q

life-threatening fungi infections for immune compromised patients?

A

Candida line infections
*Pneumocystis

216
Q

why is selective toxicity harder for fungi infections than bacteria?

A

fungi are eurkayotic and similar to human cells and there selective is harder to differentiate

217
Q

how to treat candida (oral thrush) infections?

A

antifungal - oral fluconazole

218
Q

how to treat Pneumocystis pneumonia?

A

fungal infection of lungs usually in HIV patients - co-trimoxazole (antibiotic combination)

219
Q

when is Aspergilliosis dangerous

A

released by aspergillus flavus fungi
can cause hepatocellular carcinoma
dangerous to immune comprised people (cystic fibrosis)

220
Q

chickenpox vs shingles?

A

varicella zesta virus - primary infection
herpes zoster - shingles - secondary infection

221
Q

why does herpes stay within us ?

A

lipid envelop with spikes
double-stranded DNA - mimics our own DNA

222
Q

WHEN IS VZV INFECTIOUS?

A

48 hours before spots and a couple of days (until blisters are crusted)
in nasal secretion before vesicle
in blister fluid

223
Q

small pox vs chicken pox?

A

chicken pox likes warms bits - chest
small pox - likes cooler parts of body

224
Q

signs of encephalitis?

A

seizures
confused
not able to walk properly

225
Q

most common antiviral drug?

A

Acyclovir - treatment of herpes

226
Q

serology test?
initial things detections ?

A

look for antibodies in response to virus
IgM within 1 week of onset, IgG - memory antibody appears later

227
Q

why cant viruses be detected in light microscopy?

A

Not visible in light microscopy, can’t culture as only reproduce inside live cells

228
Q

how wont pain killers work for pain of shingles?

A

need neurological treatment to treat the abnormal nerve responses in damaged nerve endings
amatryptalin

229
Q

what causes hand foot and mouth?
how to test?

A

enterovirus
PCR to test
watch out for stool- can spread

230
Q

what can enterovirus cause?

A

meningitis viral
encephalitis
endocarditis

231
Q

characterisitcs of CMV, EBV?

A

atypical lympcytes

232
Q

who is relapse of cmv dangerous for?
what does it do?

A

immuno comprismed patients
reactviation in retina - pizza
pneumonitis

233
Q

3 classes of antibtiocs ?

A
  • cell wall synthesis
  • nucleia cid synthesis
  • protein synthesis
234
Q

examples of cell wall synthesis antibtiocs ?

A

beta lactams
- pencillin
- amoxicillin
- flucloxacillin

235
Q

endogenous infections?
increases risk?

A

infections caused by patients own bacterial flora
PLASTIC - allows bacteria to form a biofilm and cause problems
related to catheter and canulla

236
Q

Preventing endogenous infections?

A

good nutrioin and hydration
antisepsis prep
remove lines as clinically possible
hand hygiene

237
Q

antibiotics for cellulitis? bacteria involved?

A

group a and group c and group g strep and s. Aureus ⇒ flucloxacillin

238
Q

antibitoics that inhibits cell wall synthesis? subgroup? examples?

A

beta lactams - penicillin
glycopeptides - vancomysin

239
Q

ratio male: female with hiv?

A

3:1

240
Q

CD4 count in HiV positive patients not on treatment ?

A

CD4 count < 200 cells/mm3

241
Q

oppurtunis infections of HIV?

A

oral candida
oral hairy leucoplakia
recurrent herpes simplex
syphalis
pnuemococcal pneumonia - PCP
multi dermatomal shingles

242
Q

Amphotericin B role?

A

antifungal
very broad spectrum and high barrier to resistance
Only IV infusion
Adverse effects - also very expensive

243
Q

common complications from HIV?

A

Kaposi sarcoma
Pneumocystis jiroveci pneumonia - FUNGAL
Candidiasis
HSV

244
Q

Lentivirus?

A

slow retrovirus family with long incubation period - HIV

245
Q

4 types of anti HIV drugs? HAART?

A

integrase inhibitors - most effective
protease inhibitors
fusion/ entry inhibitors
reverse transcriptase inhibitors

246
Q

Why is HIV highly mutative ?

A

REVERSE TRANSCRIPTASE - no error protection - error prone
Rapid replication

247
Q

Symptoms of acute retroviral syndrome?

A

Glandular fever like illness
fever
sore throat
skin rash in upper trunk

248
Q

CD4 count level of 50? risk of developing?

A

CNS lymphoma
malignant (cancer) cells form in the lymph tissue of the brain and/or spinal cord.

249
Q

what cells with CD4+

A

HELPER T CELL
REGULATORY T CELLS
DENDRITIC CELLS
macrophages

250
Q

what drives pathogenesis in HIV infection?

A

constant activation of immune system
damage to cd4 cells in gut so dangerous bacteria eneter system from gut
- antibiody response is weak and takes to months to develop the antibodies against HIV

251
Q

WHY is antiobdy response weak to hiv?

A
  • lack of protein spikes to create antibodies
  • covered in sugar molecule which lessens attachment of antibodies
252
Q

two most common bacterial causes of meningitis in adults?

A
  • Neisseria meningitidis (cocci g. negative)
  • Strep. Pneumoniae (cocci g. positive)
253
Q

agar for haemophilus influenza?

A

chocolate agar
its coccobacilli!!

254
Q

gram negative bacteria responsible for resp tract infections?

A

H influenzae

255
Q

role of lipopolysaccharide (LPS) from gram negative bacteria

A

endotoxin production

256
Q

specimens tested for with charcoal testing?

A

bacterial

257
Q

why test for IgM?

A

IgM is an acute antibody response and when detected against a virus in serum may often confirm the diagnosis of an acute infection

258
Q

hiv envelope contains?

A

RNA + capsid + RNA reverse transcriptase

259
Q

Giardia toxoplasma and Falciparum malaria are what ?

A

flagellated protozoa

260
Q

mycobacteria or bacteria Cell wall contains lipoarabinomannan?

A

mycobacteria
glycolipid that inactivate macrophages

261
Q

Broad spectrum agents promote resistance in the gut microbiome, true or false?

A

true

262
Q

staph aureus treatment?

A

flucloxacillin

263
Q

what is clostridium difficile?

A

antibiotic induced diarhea
any antibitoci beginning with a C
carbapanems - meropenem

264
Q

Co-amoxiclav role on beta lactamase?

A

beta lactamase inhibitor

265
Q

target of macrolides? examples?

A

antibiotic that inhibits ribosomal activity and protein synthesis
- Clarithromycin

266
Q

Staph infections respond to ?

A

penicillin

267
Q

antibiotic for UTI?

A

Nitrofurantoin or Trimethoprim - inhibits folate synthesis

268
Q

antibiotic for mrsa?

A

vancomysin
glycopeptide - distrupts cell wall synthesis

269
Q

common SSRI?

A

FLOUxetine - 20 mg

270
Q

List the main types of antidepressant medication and give an example of each

A
  • Selective Serotonin Reuptake inhibitors (SSRI) eg fluoxetine Sertraline
  • Tricyclic antidepressants (TCA) eg lofepramine or amitriptyline
  • Monoamine Oxidase Inhibitors (MAOI) eg selegiline
271
Q

which antidepressants are prescribed first?

A

SSRI
Tricyclic antidepressants tend not to be prescribed first line as they are more dangerous in overdose due to prolonging the QT interval of the cardiac cycle
MAOI have dangerous interactions with tyramine - found in aged cheeses, sauerkraut, cured meats, draft beer and fermented soy products

272
Q

side effects of SSRIs?

A

SSRI medication may cause heartburn and other gastrointestinal side effects, and so it is best to take it with food. Patients may also notice vivid dreams or poor sleep - take in morning !

273
Q

signs and symptoms of pneumonia?

A

Fever, sweats, malaise, “rusty sputum”, SOB, pleuritic chest pain, weakness

274
Q

pathogens in pneumonia?

A

Strep .pneumonia - gram + cocci
Coccidicides immitis (dimorphic fungi)
haemophilus influenzae - parasite causes pneumonia in HIV, CF pts

275
Q

treatment and antibiotics for osteomyelitis?

A

Flucloxacillin - strep not resistant
joint wash out

276
Q

pathogens in osteomyelitis?

A

Staph A (gram + cocci)
Strep A and B groups - s pyogenes (gram + cocci)

Enterobacter - salmonella - (gram - rod)

277
Q

treatment of chlamydia

A

its a parasite
Azithromycin (macrolides) or Doxycycline
inhibt ribosomal transcription

278
Q

4 classes acting of antibiotics acting on ribosomal inhibition?

A

MCAT

Macrolides such as erythro/clarithromycin
Chloramphenicol
Aminoglycosides like gentamicin and amikacin
Tetracyclines such as doxycycline

279
Q

which antibitoic can work against ESBL? extended spectum bacteri lactamases

A

Carbapenems are very broad spectrum and can overcome ESBL
its a beta lactam

280
Q

pathogens causing infectious endocarditis? and how do they enter?

A

Staph. aureus gains access to the blood from the skin
Strep. viridian’s gains access to the blood from the oropharynx (tooth brushing) - (cocci gram +)
Enterococci gain access to bloodstream following instrumentation of bowel (gram + cocci) - groub D strep
coagulase neg staph - IV contamination - s. epidermidis

281
Q

examples of alpha haemolytic strep ? what colour in blood agar?

A

strep. viridans
strep. pnuemonia
green!

282
Q

effect of a2 adrenoreceptor activation with noradrenaline?

A

Inhibits the release of NAd into the cleft, and reduces insulin produced from pancreas

283
Q

Effect of noradrenaline binding to B3 adrenoreceptors?

A

Increased lipolysis and relaxation of the bladder

284
Q

when should a beta blocker not be prescribed?

A

asthma !

285
Q

role of kidneys and liver with morphine?

A

Kidneys - excrete metabloites of morphine such as M6G
liver - create the metabolites of morphine with UGT (making them water soluble)

286
Q

stages of inflammation?

A
  1. vessel calibre - inflammatory cytokines mediate vasodilation - space between endothelial lining cells increases
  2. fluid exudate - vessels become leaky - fluid of vessels into tissues
  3. cellular exudate - cells leaves vessels
287
Q

conditions with central necrosis?

A

TB

288
Q

signs of parasite ?

A

granuloma and eosinophils
ACE as blood test marker

289
Q

3 stages of thrombisis?

A

1 - vasospams caused by damage
2 - primary platelet plug - VWF binds to exposed collagen - platelets bind to this
- activates
agreggetation - binds to each other
3 - platelet clotting cascade!

290
Q

formation of DVT? TREATMENT?

A

decreased blood laminar flow
warfarin

291
Q

warfarin vs aspirin?

A

warfarin - targets synthesis of clotting factors
aspirin - decrease platelet aggregation

292
Q

arterial thrombosis signs vs venous thrombosis signs?

A

aterial - cold, pale, clammy
venous - swollen tender red

293
Q

cytotoxic apoptosis?

A

CD8 binding release perforin which activates caspases

294
Q

why is apoptosis not mutagenic but necrosis is?

A

necrosis damages chromatin

295
Q

sign of benign adenoma ?

A

optic chiasm - bitemporal hemianopia

296
Q

histogenesis classifcaion?

A
  • epithelium: non glandular benign - papilloma
    non glandular malignant - carcinoma
  • connective tissue: lipoma (benign) and liposarcoma (malignant)
  • lypoid: leaukemia, lymphoma
297
Q

which carcinoma never metasasise?

A

basal cell carcinmoa

298
Q

tumor grading similarity to parent cell ?

A

differentiation
(well differentiated resemble parent cells by at least 75%)
- grade 2 slightly similar

299
Q

example of ischemia?

A

TIA

300
Q

EXAMPLE OF INFARCTION?

A

stroke

301
Q

classification of tumours?

A

behaviour and histogenesis

302
Q

example of behaviour of benign tumour?

A

slow growing
localised
exophytic - outward growth
close resemblance to normal tissue

303
Q

example of behaviour of malignant tumour?

A

basement membrane invading
rapid division - hyperdense nuclei
endophytic - inward growth
poor differentiation - little similarity to normal tissue

304
Q

characteristic of neoplastic cell?

A

autocrine growth factor
avoiding apoptosis
telemerase - prevents telemerase from shortening during each replication
own blood supply

305
Q

pathway of metastasis?

A

detachment
invasion of other tissue
invasion of Blood vessel
evasion of host defense
extravastate to distant site

306
Q

method of spread of metstatis

A

haematogenesis
lymphatic
transcolemic

Phase 2a (9 decks)

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