rojak Flashcards
(272 cards)
1
Q
type 2 pneumocytes produce?
surfactant ___long ass word___ c______
A
surfactant dipalmitoylphosphatidyl choline
2
Q
cause of plasma exudation???
A
when airway mucosa provoked. airway epithelial cells and endothelial cells exposed to inflammatory mediators (e.g. PAF & histamines), increases permeability, allow for fluid extravasation, macromolecules and cells to escape from blood vessels and into airway walls, interstitial spaces and airway lumen.
3
Q
cilia description
A
attachments: apical hools which engage w mucous cytoskeleton: 9 doublets + 2 central microtubules (axoneme) nexin links and dynein arms
4
Q
which part of inspiration and expiration is effort dependent
A
the ENTIRE inspiration dumbass and early expiration
late expiration is effort INdependent like a strong women. amt of air breathed out is the same regardless of effort. depends on compliance and elasticity of lungs and chest wall.
5
Q
fixed obstruction affect what (flow volume loop)
A
BOTH loops of inspiration and expiration. check notes
6
Q
variable obstruction got 2 types
- intrathoracic
- extrathoracic
each affect what and how (flow volume loop)
A
intrathoracic affect expiratory loop (IE)
- most severe in expiration, relieved by inspiration
- due to e.g. excess mucus
extrathoracic affect inspiratory loop (EI)
- severe in inspiratory, relieved by expiration
- due to things e.g. tumour
7
Q
what is dynamic compression, when does it occur
A
forced expiration. intrapleural pressure more positive -> intrapleural pressure > airway (alveolar)
pressure
hence, favour airway compression
8
Q
to what system/part of brain
voluntary -> ?
reflex->?
emotional->?
A
voluntary -> motor cortex
reflex-> brain stem
emotional -> limbic system
note: locked in syndrome
9
Q
hemoptysis means what
A
cough blood
10
Q
HAPE = high altitude pulmonary edema
use what drug
A
nifedipine
which fyi, is also a CCB (calcium channel blocker), which should NOT be used with b-blockers
11
Q
at which rib does the parietal pleura cross the
- midclavicular line
- midaxillary line
- scapular line
*repeat for lung
A
parietal pleura
- 8th rib
- 10th rib
- 12th rib
lung
- 6th rib
- 8th rib
- 10th rib
12
Q
isometric contraction vs isotonic contraction
match the feature!
- isovolumetric ventricular contraction/ventricular ejection
- no shortening of muscle fibers/shortening of muscle fibers
- pressure increase, valve close/ enough pressure, valve open
- associated with preload/afterload (graph)
A
isometric contraction
- isovolumetric ventricular contraction with NO shortening of muscle fibers. pressure keeps increasing due to exertion by surrounding muscles on chamber with valve close.
- length tension graph. more preload more force (Frank Starling relationship)
isotonic contraction
- ventricular ejection, shortening of muscle fibers. once sufficient pressure -> valve open (aortic and pulmonary).
- graph of muscle shortening against amt of AFTERload experienced. more afterload, less muscle shortening
13
Q
afterload how to measure
A
use diastolic arterial BP
14
Q
preload how to measure
A
end diastolic volume + pressure
OR right atrial pressure
15
Q
calcium bind what in myofilament for contraction
A
troponin c
16
Q
What pulmonary cell type is primarily involved in connective tissue synthesis?
A
type 2 pneumocytes/epithelial cells
17
Q
myalgia means what
A
muscle pain
18
Q
adenocarcinoma. 特点是什么
papillary tumour. 特点是什么
A
adeno -> GLANDULAR structure
papillary -> FINGER-LIKE projections
19
Q
squamous cell carcinoma 特点是什么
highly associated with what
A
keratinization or intercellular bridges
mutation in tp53 and CDKN2A
20
Q
Epithelioid histiocytes is what
A
MACROPHAGES
21
Q
main cellular components of Granulomatous inflammation
A
Epithelioid histiocytes and lymphocytes
note: granulomatous inflammation is the macrophage make a shield around TB
22
Q
KREBS CYCLE
your almost worst nightmare
citrate to isocitrate what enzyme
A
aconitase dumbass.
23
Q
kreb cycle
ENZYMESSSSSSSS
oxaloacetate -> citrate -> isocitrate -> a-ketoglutarate -> succincyl coa -> succinate-> fumarate -> malate -> oxaloacetate
A
- acetyl coa
- aconitase
- isocitrate dhg
- a-ketoglutarate dhg
- succinyl coa synthase
- succinate dgh
- fumarase
- malate dgh
24
Q
alternaria is what and cause what
A
plant pathogen. cause allergic rhinitis
25
which pathway of the 3 allergic thing is just built different
1. allergic rhinitis
2. asthma
3. allergic alveolitis
allergic alveolitis is non IgE mediated while the rest are IgE mediated
allergic alveolitis is IgG mediated
26
C3a and C5a do what
CHEMOKINES so they CHEMOTAXIS. they activated by proteases then increase inflammation by yelling at the cells that the bacteria is here. aka the modern billboards
27
classical pathway of complement system is how
1 4 2 3b 5b 6 7 8 9
5b 6 7 8 9 break off form MAC
3b used for opsonisation, bind to macrophage through C3b receptor
28
C5a C6 C7 C8 C9 make what for what
MAC = membrane attack complex
they attack the bacteria membrane and make a hole so the enzyme and shits can enter the bacteria. so the bacteria die bad bad
29
alternative pathway how
C3b directly bind, then the rest same same as classical pathway
30
lectin pathway (complement system) is what
C4 bind to mamose. then just continue from there.
c4 c2 c3b 5b 6 7 8 9
then same same
31
pyrexia means what
fever
32
Where is the breast located?
1. what region?
2. where does it extend from?
situated in superficial fascia of the pectoral region.
extend vertically from the 2nd to the 6th rib in the midclavicular line.
extends horizontally from lateral border of the sternum to the midaxillary line at the level of 4th costal cartilage
33
retromammary space is what
space that separates the breast from the pectoral fascia (and muscles)
34
retromammary space got what, for what
loose areolar tissue, allow for free movement of the breast on these muscles
35
areolar tissue got what, for what
loose connective tissue composed of collagen, elastic fibres and reticular fibres
for: bind skin to muscles beneath, provide support, strength and elasticity to the tissues
36
mammary gland got what
mammary gland tissue, fibrofatty tissue, connective tissue, blood vessels and lymphatics
37
lactiferous duct do what
drain each lobule, opens independently into top of nipple
38
breast blood drains into? (3 veins)
internal thoracic vein, axillary vein (mainly) and intercostal veins, along intercostal neurovascular bundle
39
suspensory ligaments? (breast)
connective tissue between gland lobules. extend from skin to pectoral fascia.
40
4 quadrants of the breast?
```
A. upper outer quadrant (superolateral)
B. upper inner (superomedial)
C. lower inner (inferomedial)
D. lower outer (inferolateral)
A | B
-----
C | D
```
41
chromosomal mis-segregration occur which stage of mitosis
metaphase
note: checkpoint kinase inhibitors are used in anti-cancer therapy => inhibit spindle assembly checkpoint @metaphase
inhibitor e.g. Taxane, cause premature mitosis, chromosomal mis-segregation and apoptosis
42
why RBC tend to burst aka lyse in low tonicity/ why WBC got more resistance
RBC no ATP bro. no energy unlike WBC. cannot transport Na+ out of cell which controls the water potential remember???
Na+/K channel is the osmolarity controller
43
hydrostatic pressure vs colloid pressure which direction
google it. but to describe:
colloid is outside vessel to inside
hydrostatic is inside vessel to outside vessel
44
tonicity vs osmolarity
osmolarity takes into account the total concentration of penetrating solutes and non-penetrating solutes, whereas tonicity takes into account the total concentration of non-freely penetrating solutes only.
tldr: tonicity care about semi-permeable membrane
45
what is SLE
Systemic lupus erythematosus. immune system attacks its own tissues, causing widespread inflammation and tissue damage in the affected organs. It can affect the joints, skin, brain, lungs, kidneys, and blood vessels.
46
what are the 7 oncoviruses?
hep B, hep C, human T lymphotropic virus, merkel cell polyomavirus, human papillomavirus, Epstein Barr virus, HHV-8
47
what are the associated cancers for the 7 oncovirus?
| hep b, hep c, human t lymphotropic virus, merkel cell polyomavirus, HPV, HHV-8, Epstein-Barr
hep b -> hepatocellular carcinoma
hep c -> hepatocellular carcinoma
human t lymphotropic virus (HTLV) -> adult T cell leukaemia
merkel cell polyomavirus -> merkel cell carcinoma
ebstein barr virus -> burkitt's lymphoma, hodgkin's lymphoma
HHV-8 -> kaposi's sarcoma
human papillomavirus -> cervical cancer, anal cancer, etc,
!!! hep c and HTLV RNA virus , the rest DNA
48
RAS pathway. what are the steps
peptide growth factors -> tyrosine kinase receptors -> receptor dimerise and cross phosphorylate -> recruit adaptor and signaling protein Grb2 + Sos (protein/exchange factor) -> RAS GTP binding protein activated -> exchange of GDP for GTP -> active (bound to plasma membrane) Ras protein -> activate protein kinase cascade
protein kinase cascade:
activated kinase 1 [RAF, MAPKKK] use gamma phosphate in ATP phosphorylate kinase 2 [MEK, MAPKK] -> kinase 2 use ATP phosphorylate kinase 3 [ERK, MAPK]
MAPK: mitogen-activated protein kinase
49
Herceptin is what
anti-HER2 antibody. block the HER2 receptor tyrosine kinase
50
cyclin dependent kinases (CDK) at M, G and S phase
M phase: cdk1 + cyclin B = m-cdk (MPF= m-phase promoting factor)
G phase: cdk2 + cyclin E = G1/S-cdk
S phase: cdk2 + cyclin A = S-cdk
51
whats the point of ERK
ERK phosphorylates and upregulate expression of Myc to express cyclin D. cyclin D bind to cdk4/6 and Rb protein to release E2F transcription factor
cyclin E transcribed -> bind to cdk2 -> drive G1 to S phase
cdk2-cyclinE phosphorylate Rb -> release more E2F -> transcribe cyclin A
cyclin A -> bind to cdk2 -> enter S phase
52
rice water stools means kena what
cholera
^ will have increased cAMP cause Cl- EFflux into gut lumen
note: usually presented with no blood in faeces.
cholera presents with large volume losses -> fluid loss, electrolyte loss
53
watery diarrhoea means what
what can cause it
non invasive, increased secretion of water and electrolytes
causes:
bacteria - vibrio cholerae, ETEC (E. coli), S. aureus
virus - norovirus, rotavirus
parasite- giardia duodenalis aka giardia intestinalis/lamblia (the parasite look like face LOL)
54
bloody diarrhoea means what
| caused by what
invasive; pathogenesis includes toxins that kill enterocytes
causes:
bacteria- shigella dysenteriae, EHEC (E. coli), Salmonella spp, Campylobacter jejuni (curved, look like w)
parasites- entamoeba histolytica
55
complication of cholera
hypokalemic metabolic acidosis
56
CD8+ T cell recognize what type of antigen (exogenous or endogenous) on what MHC
endogenous on MHC1
cd8 are your cytotoxic!!! they release the granzymes and perforin so then the cell so poof. they kill those 不是自己人
T cells cells diff: T cells recognise exogenous on MHC2!!
57
to inhibit Treg to reduce immunosuppression
anti CTLA-4 antibody: ipilimumab, tremelimumab
^ downregulation of out competition of CD28 binding to B7 (inhibits T cells)
anti PD-1 antibody: nivolumab, pembrolizumab
anti PD-L1 antibody: MPDL3280A
^ downregulation of PD-1 (Effector T cell) and PD-L1 (Treg/tumour cell) binding
therefore, more T cell, higher immuno :D
58
Beri-beri caused by what
deficiency of vitamin B1
| problem with TPP (pyruvate dehydrogenase complex)
59
beta oxidation what 4 steps.
| what do u get in the first step of b-oxidation
OHOT
oxidation, hydration, oxidation and thyolisis (aka cleavage)
first step: acyl CoA
last step: 2 acetyl CoA
60
what are some tumour suppressor genes?
p53, bRCA1, PTEN, APC, p16 INK4a, MLH1
61
function, location and associated cancer of the tumour suppressor genes
p53, BRCA1, PTEN, APC, p16 ink4A, MLH1
p53 -> cell cycle regulator, nuclear, many e.g. colon, breast, bladder, lung
BRCA1 -> cell cycle regulator, nuclear, breast & ovarian & prostate
PTEN -> tyrosine and lipid phosphatase, cytoplasmic, prostate & glioblastoma
APC -> cell signaling, cytoplasmic, colon
p16ink4A-> cell cycle regulator, nuclear, colon and others
MLH1 -> mismatch repair, nuclear, colon and gastric
62
initiator caspases that trigger cell death programme (apoptosis)
effector caspases that carry out later stages of cell death (apoptosis)
initiator: caspase 2, caspase 9, caspase 10, caspase 8
effector: caspase 3, 6, 7
63
four hypersensitivity types
Type I: reaction mediated by IgE antibodies.
* allergic rhinitis. degranulation of mast cells, release of histamine, asthma
Type II: cytotoxic reaction mediated by IgG or IgM antibodies.
*Graves disease, overactivated thyroid! not thymus! THYROID. autoimmune disease
Type III: reaction mediated by immune complexes.
*Rheumatoid arthritis, SLE
Type IV: delayed reaction mediated by cellular response.
*poison ivy rash, Rheumatoid arthritis
64
allergic asthma is what type of INFLAMMATION
**not hypersensitivity
type 1/4
65
graves disease, rheumatoid arthritis, poison ivy what type of hypersensitivity
graves disease-> type 2
rheumatoid arthritis-> type 3
poison ivy rash -> type 4
66
DiGeorge syndrome is what
highest concentration of IgM, have hypoplastic/absent thymus. T cell cannot mature, therefore no class switching to B cell. therefore, only IgM produced
67
what type of necrosis associated with acute pancreatitis
fat necrosis.
pancreatic lipase leak out of pancreas to digest fat in the abdomen. fatty acids produced can *combine with calcium to form visible chalky deposits*
68
```
what are
1. coagulative necrosis
2. caseating necrosis
3. fibrinoid necrosis
4, liquefactive necrosis
5. fat necrosis
associated with
```
1. infarction in solid organs, other than the brain e.g. myocardial infarction
* proteins denature -> form gelatinous substance -> maintain tissue architechture
2. tuberculosis, looks like cheese
* dead cells disintegrate but no completely digested -> soft, white proteinaceous mass of granular debris walled off by a distinctive inflammatory border (grannuloma)
3. deposition of antigen-antigen complexes within blood vessel
4. hypoxic infarcts in BRAIN
* dead cells digested by own enzymes -> viscous, liquid mass in cystic space (abscess formation)
5. acute pancreatitis
* activated lipase necrose fat tissue -> lesion can bind calcium to product soap/ calcium deposits
69
atrial fibrillation complication
cerebrovascular attack.
AF due to to arrhythmias cause stasis, create thrombus in left atrium. then reach brain where occludes (stroke)
70
characteristics of DVT:
____in extremities. ____ lodge within pulmonary artery -> cause _____ -> cause ____-> cause _____ since heart try to pump harder
varicosities in extremities. thrombus lodge within pulmonary artery -> cause pulmonary embolism -> cause pulmonary hypertension -> cause right ventricular failure since heart try to pump harder
71
lobar pneumonia caused by what
usually bacterial infection.
less common: viral/fungal
treatment: antimicrobial therapy
72
which pneumonia associated with
1. haemophilus influenza
2. staph aureus
3. strep cocci/pneumococci
4. TB
5. pneumocytis jiroveci
6. aspergillus
7. influenza, adenovirus, varicella
1. bronchopneumonia
* virus, has fimbriae, hair-like structure to anchor on airway epithelial cells to prevent removal by mucociliary clearance
2. bronchopneumonia
3. bronchopneumonia and *lobar pneumonia*
4. bronchopneumonia
5. interstitial pneumonia
* fungi, usually in severely immune suppressed individuals
6. interstitial pneumonia
7. interstitial pneumonia
73
bronchiectasis is what, symptoms got what
| bronchiectasis vs bronchitis
bronchiectasis: chronic, necrotising infective inflammatory condition => permanent irreversible dilatation of airways
bronchitis: inflammation of mucous membrane in bronchi
symptoms:
bronchiectasis - green/brown/blood-stained sputum (blood due to necrosis and infection), chocolate brown material in bronchiole wall since decreased elastin
bronchitis - white to yellow mucous, only if super infected then green to brown mucous, *less sputum* than bronchiectasis
74
root of right lung (hilum) posterior anterior got what
posterior: azygous vein
anterior: SVC
75
thoracic aortic aneurysm can lead to compression of what
thoracic duct and oesophagus
note: thoracic duct ascend through aortic hiatus, right of the aorta and cross to the left (posterior to oesophagus at T5)
76
use of accessory muscles for inspiration implies what
inability to use diaphragm (cannot contract) and thus, phrenic nerve injury => raised hemidiaphragm
77
phrenic nerve supply what
fibrous pericardium, diaphragmatic peritoneum, parietal pleura,
78
kussmaul respiration is what
deep, regular sighing breaths with any rate, represent respiratory compensation for metabolic acidosis (low bicarbonate)
79
women go mountain, lung how change
high altitude -> low o2 level -> HPV -> increased pulmonary resistance
due to low pAo2 -> alveolar ventilation -> reduction of PaCO2, increase pH, o2 curve shift left (respiratory alkalosis)
compensation:
respiratory alkalosis - renal compensation -> alveolar ventilation -> pao2 rise -> pH return
o2 curve shift left - RBC glycolysis -> increased production of 2,3-DPG, binds allosteric site of globin chain -> stabilize low affinity state -> shift o2 curve to RIGHT (facilitate tissue unloading)
increased hematocrit (no. of RBC) since lesser o2, stroke volume = CO x TPR and heart rate increase
80
pink frothy sputum means what
pulmonary oedema: will have impaired gas exchange, reduced lung compliance, increased pulmonary venous pressure
other symptoms: terrified, severe SOB, crackles heard upon auscultation (since inspiration opens alveoli with fluid)
81
o2 curve shift left vs right
left: loading of o2 (higher affinity of hb)
right: unloading of o2 (lower affinity of hb)
82
causes for o2 curve shift left
| + where
left:
increased pH (alkalosis)
reduced PaCO2 (bohr effect)
reduced body temp
foetal Hb, pulmonary capillaries
note: shift right just switch opposite
- maternal hb, and stored blood (detrimental), metabolically active tissue (unload o2)
83
sleep vs awake
when awake, tidal volume increases!! more respiratory muscles used when breathing (more effort)
other effects! but less
alveolar ventilation increases (increased respiratory effort)
SaO2 of arterial blood increases slightly
PaCo2 of venous blood decreased (body doesnt reach apnoeic threshold before stimulation of breathing)
breathing rate increases
84
stroke volume or Pao2 reduction by 20% more jialat
stoke volume reduction
!! only 2% of o2 transported in blood is in PaO2, 98% bound to Hb.
!!! 20% drop of SV means 20% drop of o2 delivery
85
contraction of diaphragm during inspiration or expiration
EXPIRATION BODOH
86
how to expire at super fast speed zoom zoom
breath in larger initial volume before breathing out
87
how much blood loss and what class
HR <100, BP and PP normal, RR 14-20
UOP >30, CNS slightly anxious
class 1, <740ml ~15% blood loss
88
how much blood loss and what class
HR >100, BP normal, PP decrease, RR 20-30
UOP 20-30, CNS madly anxious
class 2, 750ml-1500ml 15%-30% blood loss
note: normal blood ~5000ml
89
how much blood loss and what class
HR >120, BP and PP decrease, RR 30-40
UOP 5-15, CNS anxious confused
class 3, 1500-2000ml 30-40% blood loss
90
how much blood loss and what class
HR >140, BP and PP decrease, RR >35
UOP negligible, CNS confused and lethargic
class 4 >2000ml >40% blood loss
91
RAA system describe
angiotensinogen -> angiotensin 1 (enzyme: renine)
angiotensin 1 -> angiotensin 2 (enzyme: ACE)
bradykinin decrease -> NO decrease -> vasoconstriction
AT2 bind to AT1 -receptor -> release aldosterone -> retain SODIUM
OVERALL EFFECT: INCREASED BLOOD PRESSURE
92
types of shock (4 types)
hypovolaemic, cardiogenic, distributive, obstructive
```
note:
distributive
* septic shock, anaphylactic shock
cardiogenic
* dysfunction of heart muscle, inability to pump and supply blood to organs
```
93
anterior infarct which lead have ST elevation
V1, V2, V3 and V4
94
which lead ST elevation for lateral infarct
lead I, V5, V6, aVL
95
Von Willebrand disease is what
primary haemostatic disease.
epistaxis, prolonged gum bleed, menorrhagia (menstruation longer than 7 days), easy bruising
96
Von Gierke's disease is what
2 mutant copies of G6Pase (glucose-6-phosphatase) gene inherited. one from each parent -> G6Pase deficiency
characteristics -> low blood sugar, slow growth, large livers, short stature
97
Von Gierke's disease is what
2 mutant copies of G6Pase gene inherited. one from each parent -> G6Pase deficiency
characteristics -> low blood sugar, slow growth, large livers, short stature
98
Barrett's esophagus is what
metaplasia!!
non-keratinised stratified epithelial cells replaced by simple columnar epithelial cells when exposed to stomach acid (E.G. during stomach acid reflux)
note: metaplasia is reversible!!
99
anomaly during metaphase -> daughter cells have unequal amount of DNA
deficiencies in BUB kinase signaling
- BUB kinase generate checkpoint signals during metaphase when kinetochores are not bound to microtubules
- prevent anaphase from taking place until all kinetochore attached to MT
- deficiency = premature anaphase
100
amphitelic attachment of microtubule to chromosome kinetochore normal anot
yes. amphitelic literally means proper attachment of spindle attachment
101
abberrant cytokinesis -> unequal amount of DNA occurs when
cytokinesis AFTER mitosis
102
transcription of DNA occur which direction
5' to 3'
103
binding of elF2 to GTP and Met-tRNA involved in what process
translation!!
104
what is profilin
profilin = protein assist microfilament elongation
*exchanges ADP for ATP on actin monomers -> convert to readily polymerizing form
105
how does polymerisation of MT occur
nucleation: require tubulin, Mg, GTP, 37 degrees. SLOW
elongation: polymerisation of dimer, happens at PLUS END if GTP present
note: MT does not keep growing if GDP is at the plus end
106
5 types of intermediate filament
type 1 and 2: acidic keratin (type 1) and basic keratin (type 2)
* found in epithelial cells (bladder, skin, etc)
type 3: cell types include
* vimentin (fibroblasts, endothelial cells, leukocytes)
* desmins (desmosomes e.g. cardiac muscle, skeletal muscle)
* glial fibrillary acidic protein GFAP (in astrocytes)
* peripherin (peripheral nerve fibers)
type 4: neurofilament
* heavy, medium, low
* modifiers refer to molecular weight of protein, mainly in axonal cells
type 5: lamins
* filamentous support inside inner nuclear membrane
* vital for reformation of nuclear envelope after cell division
107
what does gelsolin do to microfilament aka actin
gelsolin binds to +end!
gelsolin involved in severing and capping microfilament -> increase number of filaments avail -> increase TOTAL RATE of elongation
note:
ARP 2/3 and WASP assist in nucleation of microfilament
filamin assist microfilament bundling
108
prokaryote DNA replication how many origin
ONLY ONE. remember its a CIRCLE!! so only form ONE replication bubble
109
reduced protein in interstitium, pressure how
| increased protein in capillaries, pressure how
1. (reduced protein, interstitium) interstitial colloid osmotic pressure decreases
note: therefore, less water pulled into of interstitium, into the blood vessel.
INCREASED circulatory volume
2. (increased protein, capillaries) plasma colloid osmotic pressure increase, retain fluid in plasma
110
wtf are schwann cells
main glial cells of the peripheral nervous system which wrap around axons of motor and sensory neurons to form the myelin sheath.
tldr: MYELIN SHEATH `
111
schwann cell do what
allow for myelination -> allow for high AP conduction velocity 150m/s due to saltatory conduction
note: unmyelinated only 0.5-10m/s only
112
excess acetylcholine do what to your sweat
INCREASE production!! sweat glands stimulated by secretion of acetylcholine
113
organ abscess caused by what
clue: entamoeba
entamoeba migration to organs through bloodstream after penetrating enteric mucosa
114
acute exacerbation of asthma use
1. short acting muscarinic agonist or antagonist to treat
2. long acting beta-adrenergic antagonists or agonist to alleviate bronchial smooth muscle constriction
1. ANTAGONIST!! we want to block PARAsympathetic pathways to lungs -> inhibition of bronchoconstriction
2. agonist!! initiate sympathetic -> bronchodilation
115
dropping eyelids, constricted pupil, dryness of face on right side is what syndrome
right sided Horner's syndrome
| * arises from lesion of sympathetic chain at T1/T2
116
localised cholecystitis (redness and swelling of gallbladder) affect what
greater splanchnic nerve
symptom: right upper quadrant pain
117
axillary artery
1. branch of what artery
2. supply what
subclavian artery. supply axilla and upper limb
118
which organism NOT causative agent of IE
1. eikenella corrodens
2. acinetobacter baumannii
3. viridans streptococcus
4. aggregatibacter actinomycetemcomitans
acinetobacter baumannii
119
b1, b2-receptor where
b1-> on heart, facilitate sympathetic activation @SA node
| b2-> in lungs
120
what condition or mechanism failure cause syncope (fainting)
lack of a1 adrenoceptor stimulation.
syncope -> hypotension, lack of perfusion to brain
^ caused by insufficient CO increase/insufficient peripheral vascular resistance
MAP = CO x TPR
note:
a1 adrenoreceptor found on PERIpheral blood vessels -> activated for vasoconstriction
b2 adrenoreceptor found on blood vessels -> activated for vasodilation -> decrease BP
hypotension decrease baroreceptor stimulation
121
lowered pH caused by ketone bodies detected by?
chemoreceptors
122
baroreceptor describe
1. via what
2. effects if increase
3. where
via vagus nerve. if increase baroreceptor firing, INCREASE parasymp, DECREASE symp, DECREASED HR
at aortic arch and carotid sinus
stimulated by arterial pressure drop (BP drop)
note: to test, use valsava
* increased intrathoracic pressure, decreased venous return, decreased cardiac output, therefore, DECREASE IN ARTERIOLE PRESSURE, parasymp increase, symp decrease, HR increase
123
what affects sensitivity of baroreceptors
chronic hypertension
124
peripheral and central chemoreceptors
1. where
2. respond to what
peripheral
1. aortic arch & carotid bodies
2. hypoxic (low PaO2), high PaCO2, low blood pH
central
1. surface of medulla
2. KETONE BODIES, high PaCO2, low pH in cerebrospinal fluid
125
b1, b2-receptor where
b1-> on heart, facilitate sympathetic activation @SA node
| b2-> in lungs
126
smokers! bronchus! got increased density of blood vessel?
YES!
| note: there will be a proliferation of smooth muscle myocytes as well!
127
oedema cause in MALNOURISHED
malnourish-> proteolysis (to generate aa for metabolism for energy) -> decreased serum albumin levels -> DECREASE COLLOID OSMOSTIC PRESSURE (aka low blood protein level) -> oedema
128
multiple sclerosis how affect neuron
autoimmune disease where Schwann cells are attacked. therefore reduce speed of conductance of neuron
129
multiple sclerosis how affect neuron
autoimmune disease where Schwann cells are attacked. therefore reduce speed of conductance of neuron
130
anti CTLA-4 antibody mechanism
upregulate activation of naive T cells by dendritic cells
note: anti CTLA-4 antibodies used as checkpoint therapy against cancer
CTLA-4 found on naive T cell soon after activation
CTLA + B7 (on dendritic) binding downregulate activation of T cell
***CTLA-4 expressed on Treg = downregulate ability of dendritic cells to present antigen
131
pulmonary surfactant first formation in baby (how many weeks, which period)
when does surfactant-secreting type 2 pneumocytes differentiate the most (what period)
terminal saccular period
132
key difference between COX-1 and COX-2
COX-1 found in healthy individuals
| COX-2 switched on during inflammation and pain
133
RNA polymerase I, II and III used for what type of RNA
I: rRNA
II: mRNA
III: tRNA and 5S RNA
134
tamoxifen for what
breast cancer. block estrogen receptor
135
anticodon that tRNA delivers methionine?
CAU (5'-3')
REMEMBER DIRECTION
136
does translation use GTP/ATP and what enzyme
GTP + peptidyl transferase
137
translation: preinitiation complex involve binding to what subunit
60S subunit
1. Dissociation of ribosome into 40S + 60S subunit
2. Assembly of preinitiation complex
* Met- tRNA (since start codon is always AUG)
* eIFs (eukaryote initiation factor)
* 40S subunit
3. Binding of mRNA to preinitiation complex
4. Binding of 60S subunit
138
what do the following meds act on what in bacteria
1. streptomycin
2. tetracyclin
3. erthromycin
4. chloramphenicol
5. puromycin
1. streptomycin - inhibit initiation
2. tetracyclin - inhibit aa-tra binding
3. erthromycin - inhibit translocation of ribosome along mRNA
4. chloramphenicol - inhibits peptidyl transferase
5. puromycin - terminates elongation prematurely
139
```
CARCINOGENESIS
effect and source of
1. benzo [a] pyrene
2. aflatoxin B2 from Aspergillus flavus mold
3. 2-napthylamine
4. pyrimidine (thymine dimers)
5. free radicals
```
1. benzo [a] pyrene
* DNA adducts, pollutants
2. aflatoxin B2 from Aspergillus flavus mold
* liver carcinogen, poorly stored grains and peanuts
3. 2-napthylamine
* bladder cancer, dye-industry
4. pyrimidine (thymine dimers)
* skin cancer, solar radiation
5. free radicals
* strand breaks, base modifications, ionising radiation
140
hybridisation stringency increases with?
higher temp and DECREASE in Na+ conc
note: at high stringency, only DNA sequences which are EXACTLY identical will bind
141
which end does elongation of MT occur preferentially?
plus end
142
MT associated proteins bind to MT for?
1. to stabilize them
2. to cross-link them
3. attach them to other cellular components: membranes, intermediate filaments, other MT
143
actin: got 2 types, what are they
G-actin (globular) - actin monomers
*ATP bind w actin monomers = ATP hydrolysed => ADP-actin and Pi
F-actin (filamentous) - actin filaments
144
Cellular poisons against actin filaments
!! active at low concentration
1. cytochalasin - inihibit polyermerisation/depolymerisation
2. latrunculin - inhibit polymerisation
3. phalloidin - binds to and stabilise F-actin
145
capping proteins, 2 types :
+end and -end
name some examples
+end: cap z, gelsolin, fragmin/severin
| -end: tropomodulin, arp complex
146
filopodia is what
tight parallel bundles
note: formation by actin polymerisation, bundling and cross-linking
note: stress fibre creates tension and facilitates retraction of cell
147
profilin vs thymosin
profilin help to take the G-actin to F-actin: yay! polymerisation!!
thymosin block the G-acting, kidnapping!: OH NO! no polymerisation
148
lamellipodia
sheet like protrusion
note: formation facilitated by arp2/3 complex (branching) and cofilin (disassembly)
note: stress fibre creates tension and facilitates retraction of cell
149
intracellular protein transport 3 types
1. gated transport
2. protein translocation
3. vesicular transport
150
various coat proteins that involve in shaping vesicles include?
COPI, COPII, Clathrin
151
Marfan Syndrom
Fibrillin 1 mutation
* predispose aortic rupture
* elastic fibre
152
Osteoarthritis due to what
loss of ECM (degenerative disease), due to cleavage and loss and aggrecans
153
cystic fibrosis
CFTR gene, degradation of transmembrane receptor
154
intermediate mesoderm become what
kidney, gonads, adrenal cortex
155
heart nerve fibres & area of referred pain
T1-5
| left precordium n left upper limb
156
stomach nerve fibres n area of referred pain
T5-9
| lower chest n abdominal wall
157
gallbladder nerve fibres
T5-9,
lower chest and abdominal wall
note:
if infection spread to peripheral diaphragm and anterior abdominal wall
*6th-11th ics nerves, R upper quadrant of abdominal wall, all the way to inferior angle of scapula
if infection spread to CENTRAL diaphragm
*C3-C5, right shoulder
158
posterior parietal cortex required for what, associated with what syndrome
required for attention!!!
associated with hemispatial neglect syndrome if damaged.
note: hemispatial neglect syndrome = when asked to draw clock, left blank but right half filled
159
what do the following metabolic poisons do
1. rotenone
2. malonate
3. cyanide and azide
4. carbon monoxide
5. oligomycin
6. dinitrophenol and thermogenin/UCP-1
7. arsenite and mercury
1. rotenone - inhibit NADH dhg
2. malonate - competitive inhibitor of succinate dhg
3. cyanide and azide - bind to ferric (Fe3+) in cytochrome oxidase
4. carbon monoxide - bind to ferrous (Fe2+) in cytochrome oxidase
5. oligomycin - binds to stalk region in ATP synthase
6. dinitrophenol and thermogenin/UCP-1 - decoupling of ATP synthase
7. arsenite and mercury - readily inhibits pyruvate dhg
160
tissue distribution of hexokinase I and glucokinase (aka hexokinase IV)
hexokinase I: skeletal muscles
| glucokinase aka hexokinase IV: liver cells (hepatocytes), pancreas B cells
161
hexokinase I vs glucokinase (aka hexokinase IV)
1. glucose affinity
2. regulation
1. glucose affinity
hexokinase:
high glucose affinity (LOWER Km),
effective at LOW conc. ineffective at high conc
LOWER binding capacity (LOWER Vmax)
glucokinase:
LOW glucose affinity (HIGHER Km)
effective at HIGH conc, ineffective at low conc
HIGHER binding capacity (higher Vmax)
2. regulation
hexokinase:
allosteric inhibition by G6P
glucokinase:
inhibition by glucagon
*less sensitive to G6P inhibition
activated by insulin
162
creatine phosphate importance?
| process catalyzed by?
source of ATP in muscles, buffer demands for ATP during intense exercise
catalyzed by creatine kinase
note: if muscle is damaged, creatine kinase leaks into bloodstream
!!!!creatine KINASE useful diagnostic marker for muscle injuries
*(can be used to diagnose/evaluate/discover)
elevated = MI, extent of muscular disease, chest pain, carrier of muscular dystrophy [duchenne]
163
embryology
what week to what week
1. pseudoglandular period
2. canalicular period
3. terminal saccular period
4. alveolar period
1. week 5-17
2. week 16-27
3. week 24-38
4. week 36-8 years
164
end systolic volume determined by closure of what valve
aorticcc
165
brain reliant on what metabolism
GLUCOSEEE!!
cannot use b-oxidation of fat in brain!
166
net yield of krebs cycle
6NADH, 2GTP, 2FADH, 4CO2
^for one GLUCOSE not one cycle
note: energy yield 24 ATP
* 6 x3 + 2x2 + 2x2 =24
167
which is the SOLE insoluble protein in mitochondrial matrix
succinate dehydrogenase
| *found on inner mito membrane
168
NADH transport from cytosol to inside mito matrix how (2 shuttles)
glycerol-phosphate & malate aspartate
169
glycerol phosphate vs malate aspartate
1. found where
2. atp yield per nadh
3. pass electron to
note: shuttles above transport NADH from cytosol into mito matrix
1. found where
glycerol phosphate- skeletal muscle and brain
malate aspartate - liver, kidney and heart
2. atp yield per nadh
gly phos - 1.5
mal asp - 2.5
3. pass electron to
gly phos - FADH2 (skips etc 1)
mal asp - NADH
170
describe how gly-pho shuttle works
cytosol glycerol-3-phosphate dhg
*transfer electron from nadh to glyercol-3-phosphate
then mitochondrial glycerol-3-phosphate
*electron transferred to FAD -> then passed to co-enzyme Q (ETC)
171
ETC describe
electron move from what order
how many complex and mobile carrier
```
NADH dhg (NADH) or succinate dhg (FADH2) -> ubiquinone (co-enzyme Q) -> cytochrome b-cl -> cytochrome c -> cytochrome oxidase
with o2 as the terminal electron acceptor
```
3 complexes, 2 mobile carriers
172
atp synthase structure describe
F1 (part projecting into matrix)
- A, B, Y subunit
F0 (membrane bound part)
- abc subunit
note:
c and Y rotate
a, b, A, B do not rotate
A, B change conformation to generate ATP
watch youtube video to visualise mechanism!
173
5 reactions of gluconeogenesis (what catalyst)
1. pyruvate -> oxaloactetate
2. oxaloacetate -> phosphoenolpyruvate
3. fructose-1,6-biphosphate-> fructose-6 phosphate
4. fructose-6 phosphate -> glucose-6-phosphate
5. glucose-6-phosphate -> glucose
1. pyruvate carboxylase
*allosterically activated by acetyl-coa
(break down too much glucose -> make more glucose)
2. phosphoenolpyruvate carboxykinase
3. fructose-1,6-biphosphatase
4. phosphoglucoisomerase
5. glucose-6-phosphatase (
174
```
b-oxidation,
how much ATP from
1 acetyl coa
1 fadh2
1 nadh
```
acetyl coa -> TWELVE 12 SHI ER!!
fadh2-> 2
nadh -> 3
175
how to find out how many b-oxidation cycle it need to go through
and how many acetyl coa
b-oxidation cycles: (no. of carbon of fatty acid - 2) / 2
| acetyl coa: no. of carbon fatty acid/2
176
4 steps of lipogenesis (fat acid synthesis) on top of the transference of carbon groups to acyl carrier protein (ACP)
* 1 malonyl-acp (3c)/cycle
* 1 acetyl-acp (2c)
CRDR
condensation, reduction, dehydration, reduction
(2NADPH used)
^ OI GOT A P CUZ THIS IS SYNTHESIS NOT DEGRADATION OK
rmb SymPathetic
177
MCADD
medium chain acyl coenzyme a dhg deficiency
treatment?
treatment:
1. never go w/o food more than 10-12 hours
2. high carbs diet
3. IV glucose if cannot consume glucose (vomiting)
* note: autosomal recessive
pt unable to oxidase fats as energy source
178
cholesterol synthesis molecule steps
Mevalonate (C6) -> Isopentyl (C5) -> Geranyl (C10) -> Farnesyl (C15) -> Squalene (C30) -> Lanosterol (C30) -> Cholesterol (C27)
mevalonate is germany's first student loan company
note: require NADPH cofactor, ATP, Mg and Mn
179
cholesterol derivatives (3 main types)
steroids
vitamin D
bile salts (major breakdown product of cholesterol)
180
statin vs resins
statins inhibit hmg coa reductase (cholesterol)
| resins sequesters bile acid - cholesterol complex
181
what can only use glucose as metabolic source (got 2)
brain and NERVOUS TISSUE
| * ok by right can use ketone also but like they acidic and too much will kena toxic and die
182
in FH (familial hypercholesterolamia), whats the problem
genetic condition, cannot take up LDL cuz the LDLR spoil
183
hmg-coa inhibitor or hmg-coa reductase inhibitor correct
REDUCTASE CHILD!! MUST HAVE THE WORD REDUCTASEEEEEE
184
neural crest cells (neuroectoderm) give rise to what
schwann cells, sensory and autonomic ganglion, adrenal medulla, melanocytes (MAGS), retina, posterior pituitary gland
185
broca's aphasia vs wernicke;s aphasia
broca: broken speech, but can understand
wernicke: good speed, but cannot understand
186
how many nerves and vertebrae in cervical?
8 nerves, 7 vertebrae
187
where does spinal cord end
L2 at conus medullaris
continues as the cauda equina
note: lumbar puncture performed at L4/5 since spinal cord already ended.
188
grey matter contain what
specify
1. dorsal horn
2. lateral horn
3. ventral horn
cell bodies!
1. sensory neurons
2. autonomic neurons
3. motor neurons
189
white matter contain what
specify
1. dorsal column/funiculus
2. lateral column/funiculus
3. ventral column/funiculus
axons and myelin sheath
1. sensory/ascending tracts
2. autonomic, ascending and descending tracts
3. motor/descending tracts
190
where does decussation occur
just before the junction between the medulla oblongata and the spinal cord
191
lesion to motor pathway vs lesion to sensory pathway
1. lesion BEFORE decussation
2. lesion AFTER decussation
deficit where
1. BEFORE
motor - opposite
sensory - same
2. AFTER
motor- same
sensory - opposite
192
somatic motor vs visceral motor
| *transmit impulse where
somatic- skeletal muscles
| visceral - smooth muscles and glands
193
visceral sensory transmit what from where
transmit pain/subconscious visceral reflex sensation from hollow vessels, internal organs to glands to the CNS
note: visceral sensory are NOT part of ANS
194
STRUCTURE OF SPINAL NERVE
dorsal root vs ventral root
dorsal ramus vs ventral ramus
ROOT:
dorsal - general sensory fibres to posterior horn of spinal cord
ventral - somatic motor fibres from cell bodies in spinal cord
^ these will unite to form MIXED SPINAL NERVE
RAMUS:
dorsal - supply nerve fibres to synovial joint of vertebral column, deep muscles of back and overlying skin
ventral - supply anterior and lateral trunk, upper and lower limbs
195
ANS step by step
control centre at hypothalamus -> preganglionic fibres project form spinal cord -> synapse at autonomic ganglia -> post-ganglionic fibres emerge and from terminal networks in target tissues/organs
tldr: hypothalamus -> preganglionic -> synapse :D -> post ganglionic
196
white ramus communicans vs grey ramus communicans
white ramus communicans
*carries preganglionic sympathetic fibers to sympathetic chain
grey ramus communicans
*carries postganglionic sympathetic fibers rejoining the spinal nerve
197
referred pain
| visceral afferent fibres synapse at sympathetic ganglia???
NO. THEY JUST CONTINUE TO SPINAL CORD THROUGH DORSAL ROOT!!!
Visceral afferent fibres run with sympathetic efferent, DO NOT SYNAPSE at sympathetic ganglia, continue to to spinal cord through DORSAL ROOT.
-Dorsal root ganglia have both somatic and visceral sensory neurones→ causes mixing up, body misperceives visceral organ pain as skin pain
198
shen me shi
- m line
- z disc
- a band
- i band
- h zone
M-line: attachment for thick filaments (myosin)
Z-disc: dense protein that serve as an attachment for thin filament (actin), multiple discs form a Z-line that separates sarcomeres
A band: dark bands of thick myosin filaments
I band: light bands of thin actin filaments (not covered by thick filaments)
H zone/band: region composed of only thick filaments (with no overlap with thin filaments)
199
when calcium bind to troponin, what happens
cause tropomyosin to move, thus freeing myosin
200
cross bridge cycling
go and look at image
201
b- lymphocytes express what cd
cd19 and cd20
202
germinal centres what happen
b cell can differentiate into plasma cell and memory cell
note:
SIGNAL 1 - MHCII and TCR, costimulation by B7 and CD28 (T cell activation)
SIGNAL 2 - process directed by Tfh -> provide direct co stimulation of B cell via CD40R (B cell) and CD40L (on T cell)
203
somatic hypermutation vs class switching
polyclonal vs monoclonal
```
somatic hypermutation: change in VARIABLE region, increase AFFINITY of ab to antigen
class switching: change in CONSTANT (Fc) region, change in effector function (e.g. IgM-> IgG)
```
polyclonal: ab from different b cell lineages able to recognise multiple different epitopes of a single antigen
monoclonal: ab clones of same parent cell, only recognise single epitope of single antigen
tldr; polyclonal = can recognise many many epitope. monoclonal = dumb fks only can recognise that one
204
which Ig can cross placenta
IgG
205
when IgA produced
body secretions in mucosal areas e.g. gut, respiratory tract, breast milk
note: prevent mucosal surface from colonisation by pathogens
206
what composition of cell, highest survival rate for cancer
Th1 high, Th17 LOW
207
mutant foxp3 transcription factor how
IPEX
note: foxp3 impt for treg
208
Tcells have what CD
ALL HAVE CD3!!!! and CD28
note: cd28 is a receptor for CD80/86, which is needed for TCELL ACTIVATION
209
cortex vs medulla (which part of thymus)
cortex: outer part of thymus
medulla: inner part of thymus
210
3 signals of CD4+ T cell
1. mhc to tcr
2. cd80/86 to CD28
4. specific cytokine e.g. IL-4 for Th2
211
3 signals of CD4+ T cell
1. mhc to tcr
2. cd80/86 to CD28
4. specific cytokine e.g. IL-4 for Th2
212
Gs protein vs Gi protein
Gs ACTIVATES adenylate cyclase, therefore INCREASE cAMP production
Gi do opposite
note:
Gq activates PLC-beta, increase diacylglycerol, increase IP3, increase protein kinase c activity, increase CYTOPLASMIC CA2+
By alters ion channel function, ACTIVATES PI3K and PLC-beta
213
Gq vs By
Gq activate PLC-beta which increase diacylglycerol, increase IP3, increase Ca2+, increase protein kinase c activity
By affect ion channel function, activate PI3K and PLC-beta
note: Gs ACTIVATES adenylate cyclase, therefore INCREASE cAMP production
214
is the loss of p63 staining myoepithelial cells in ducts and lobules normal?
NO! myoepithelial cells (in breast) usually stain positive for p63
215
superior and posterior boundary of posterior mediastinum
superior: transverse line from sternal angle to lower border of T4
posterior: TV to TXII
216
cervical oesophagus start where
C6, end at jugular notch
217
what level hemiazygos vein cross to the right to drain into azygous vein
t8/9
cross to the right BEHIND aorta, thoracic duct and oesophagus
note: vs accessory hemiazygous vein => cross at T7/8
218
is accessory hemiazygous vein anterior or posterior to thoracic aorta
posterior
219
where does the thoracic lymphatic drainage start
L2 from cisterna chyli!!
note: it travels on the RIGHT of thoracic aorta and oesophagus, LEFT of azygous vein
220
thoracic lymphatic drainage when cross midline to left (via behind oesophagus)
T5
it then passes over the dome of left pleura and anterior to the left vertebral and subclavian arteries
221
what goes through aortic hiatus
T12!! azygous vein, aorta and thoracic duct
222
thoracic duct drain which one
option1: upper left body and whole body below diaphragm
option2: upper right body
OPTION 1: upper left body and whole body below diaphragm!!
upper right body is by right lymphatic duct
223
sympathetic nerve how to enter abdomen (where)
pierce crus of diaphragm or by passing posterior to the medial arcuate ligament
224
infectious dose vs infectivity
infectious dose = ability of bacterium to initiate infections
infectivity = ability of bacterium to initiate infections
therefore, lower infectious dose -> HIGHER infectivity
225
what are the hall marks of cancer (10)
1. growth signal autonomy
2. evasion of growth inhibitory signal
3. avoiding immune destruction
4. unlimited replicative potential
5. tumour-promoting inflammation
6. invasion and metastasis
7. angiogenesis
8. genome instability and mutation
9. evasion of cell death
10. reprogramming energy metabolism
226
dementia and cachexia what happen to the cell? (e.g. hypertrophy??)
atrophy (decrease SIZE of cells)
NOT NUMBER!!
227
necrosis vs apotosis
1. need ATP
2. most common outcome
3. inflammation?
4. characteristics
1. necrosis - NO NEED ATP, apoptosis - YES
2. necrosis - i die, we all tie tgt (damage surrounding tissue), apoptosis - single cell death
3. necrosis - YES INFLAMMATION, apoptosis - NO inflammation
4. characteristics
necrosis - irreversible plasma membrane damage with organelle breakdown
apoptosis - condensation into apoptotic bodies -> rapid phagocytosis (membranes left intact)
228
...sarcoma means what and spread by what
malignant mesenchymal tumour, VASCULAR spread
vs carcinoma: malignant EPITHELIAL tumour, LYMPHATIC spread
229
cushing disease is waht
Cushing disease is a condition in which the pituitary gland releases too much adrenocorticotropic hormone (ACTH)
230
HIV coreceptor is what
CCR5 (mostly) - macrophages, DC, Tcells
CXCR4 (mutated) - T cells
bind to GP 120
231
which fungi most likely to develop after antibiotic therapy
candida albicans
232
A patient presents with white plaques on the buccal mucosa and tongue. Upon further investigation, it is confirmed to be oral thrush, or oropharyngeal candidiasis. What is a predisposing factor?
antibiotic therapy
233
what fungi can kena because of impaired cell-mediated immunity
candida (mucosal infection) and cryptococcus
234
which fungi can kena cause of
1. diabetes
2. impaired mucosa, physical breach of epithelial barriers
3. high dose corticosteroids (organ transplant)
4. HIV
1. candida
2. candida
3. aspergillus
4. cryptococcus
235
primary pathogens (4 types)
Coccidioides immitis
Histoplasma capsulatum
Blastomyces dermatitidis
Paracocidioides brasiliensis
236
what is candida defence
experience starvation in phagolysosome -> germination and escape
*which is prevented by neutrophils
237
aspergillus aka mold can kena from where
airborne and ubiquitous
note:
aspergilloma in cavity lung disease
chronic necrotising aspergillosis in chronic lung disease/mild immunocompromised
Invasive pulmonary aspergillosis in immunocompromised
Allergic bronchopulmonary aspergillosis (bronchiectasis with pulmonary consolidation) in asthma
238
body defence to aspergillus
NETs
239
cryptococcus aka yeast from where
soil, trees, airborne!!
ENCAPSULATED yeast most common lethal fungal infection in pt with AIDS worldwide
240
how body defend against cryptococcus
use alveolar macrophages and cd4 th1 response to clear
*usually fungi would multiply in macrophage phagosome and after that escape
241
antifungal drugs do what
1. azole, polyene, allylamines
2. pyrimidine analogues
3. echinocandins
1. ergosterol (cell membrane of fungi)
2. dna synthesis
3. cell wall (chitin and glucans)
* non-specific inhibition of b-1,3 glucan synthase
242
NK cell for what type of infection? viral fungal or bacteria
VIRAL
243
Fever, bloody diarrhoea (dysentery), abdominal pain, liver abscess . symptoms of what
esp if trophozoites with endocytosed RBCs
entamoeba histolytica
244
taenia spp. (cestode) what type in pig in beef
pig: t. solium
* cause cysticercosis (EPILEPSY)
beef: t. saginata
245
plasmodium spp.
1. nucleus look like what
2. can cause what
head phone, ring shaped
cause malaria: fever, headache, anaemia, splenomegaly
Falciparum malaria - infected RBCs stick to capillary walls, blocking them, thus leading to ischaemia of brain, kidney, lungs
246
what cause intermittent/spiking fever, pancytopenia, hepatosplenomegaly, Kala-azar (black fever - skin hyperpigmentation), weight loss,
skin lesions and disfiguring ulceration
leishmania spp. (got tail, look like sperm but the head look like beauty blender)
247
bloatedness, flatulence, steatorrhea caused y what
giardia lamblia (look like face)
248
burning, itching of inflamed cervix (which appears erythematous with petechiae), frothy, yellow-green, foul-smelling discharge
Trichomonas vaginalis (motile pear-shaped trophozoites)
249
diarrhoea and malabsorption
Strongyloidiasis
| nematode
250
Cause schistosomiasis - hepatosplenomegaly, liver cirrhosis and fibrosis, portal hypertension
lead to squamous cell carcinoma of the bladder and pulmonary hypertension
what is it
Schistosoma spp. (trematode)
251
pathway of temperature signal
temperature (sensor in skin) -> AFferent signal into spinal cord via Lissauer's tract -> passed to LATERAL spinothalamic tract -> hypothalamus (pre-optic area, dorsal hypothalamus) -> central heat receptors in hypothalamus -> signal to tissue for homeostasis
252
what can cause saddle back fever
dengue, leptospirosis, legionnaire's disease
253
what can cause spiking fever
TB, abscess, schistosomiasiss
254
what cause remitting fever
amoebiasis, malaria, kawasaki disease
255
what cause longer periodicity fever
pel-ebstein fever from lymphoma
256
A 33-year-old patient is suffering from a sudden occlusion at the origin of the descending (thoracic) aorta.
This condition would most likely decrease blood flow in which of the following intercostal arteries?
lower nine posterior
ICS 3-11
first 2 is by costocervical trunk
257
aortic hiatus what arcuate ligament
MEDIAN
258
alveolar dead space why
not enough BLOOD SUPPLY
259
requirements for effective airflow
Alveoli open
Airways patent
Pleural layers sliding easily.
260
airway vs respiratory units (NORMAL)
airway: 70% macrophages, 30% neutrophil
respiratory: 90% macrophages, 10% neutrophil
note: COPD 30% macrophage, 70% neutrophil
261
pulmonary oedema -> restrictive or obstructive?
RESTRICTIVEEEEEE, will decrease lung compliance
poor left ventricular function → excess blood in pulmonary vasculature → vascular engorgement, extravasation due to increased hydrostatic pressure and pulmonary oedema → makes lung stiffer and reduce compliance
262
MEN2 caus what tumour
thyroid gland, adrenal gland, and parathyroid glands.
263
which MMR (mismatch repair) genes work cooperatively
for DNA
MLH1 + PMS2
| MLH2 + MSH6
264
what is MSI (microsatellite instability)
repeated DNA motifs, usually in non-coding DNA
265
lynch syndrome aka HNPCC ( Hereditary Non-Polyposis Colon Cancer)
Caused by mutations in MMR genes, especially MLH1, MSH2, and MSH6, which leads to microsatellite instability
Patients develop colorectal and endometrial cancer
Autosomal dominant inheritance
266
how to treat breast cancer (mutation in BRCA1 and BRCA2)
PARP inhibitor
267
steps of metastasis (5 steps)
1. invasion (EMT)
2. intravasation (tumour cell enter blood stream, transendothelial migration)
3. transport/dissemination (sheer stress survival)
4. extravasation (transendothelial migration)
5. metastatic colonization
268
EMT transcription factor upregulate/downregulate what shits
upregulate N-cad and MMPs
| downregulate E-cad
269
Dyskeratosis congenita (DC) caused by what
mutation in telomerase or telomere binding sheltering complex
!!=> premature aging and stem cell failure
270
p53 regulated by what ubiquitin ligase
MDM2
271
WHATS THAT SOUND?
radiate to carotids, late DIASTOLIC murmur (s3)
aortic REGURGITATION
diastolic -> aortic regu or mitral stenosis
mitral: mid-diastolic murmur
272
WHATS THAT SOUND
| systolic murmur + radiate to carotids
aortic stenosis since SYSTOLIC + carotids
systolic -> aortic stenosis/ mitral regur
