year 1 medicine revision

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  • Created by: Patrick
  • Created on: 03-05-14 16:46
What is haematocrit and what are its normal margins?
Ratio of RBC volume: total volume. 30-70%
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haemoglobin levels (Hb)
men: 130-180g/L. women: 115-165g/L
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mean cell volume
10x (hameatocrit/RBC count). normal range 76-100FL
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mean cell haemoglobin
average mass of haemaglobin/cell. Haemoglobinx10/RBC. normal range 26-32 pico grams
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mean cell haemaglobin [..]
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2-4 micrometers. 7-14 day lifespan
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blood group A
B antibodies, A antigens
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blood group B
A antibodies, B antigens
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blood group AB
no antibodies, AB antigens
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blood group O
AB antibodies, no antigens
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erythrocyte formation
Myeloid cell>BFU>CFU>pro-erythroblast>erythroblast>normoblast>reticulocyte>RBC. normoblast Denucleated by macrophages. GATA-1 and EPO
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platelet formation
myeloid>megakaryocyte>platelet. GATA-1 and TPO
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myeloid?CFU-GM>promyleocyte>myelocyte>neutrophil. Monocytes form from CFU. Requires PU1, G-CSF and c/EMPa
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what stimulates EPO release?
low O2 tension in PCT
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causes of iron deficiency anaemia (microcytic, hypochromic anaemia)
diet, malabsorption, bleeding, menzes, pregnancy, worms, GI bleed.
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macrocytic anaemia with ataxia and dementia
B12/folate deficiency. Caused by diet/alcohol. serum B12, folate and Schilling test
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macrocytic and haemolytic anaemia?
pernicious anaemia (no IF from stomach= no binding for absorption in terminal ileum)
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acute drop in haemoglobin
acute bleeding, rapid haemolysis, poisoning and chronic
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mild macrocytic normachromic and leukoerythroblastic film.
bone marrow failure
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normacytic normachromic anaemia with B12 deficiency
liver failure. alcohol suppresses marrow and causes bleeding
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causes of haemolytic anaemia
sickle cell, autoimmune, malaria, hereditary spherocytosis
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normacytic normachromic anaemia and raised renal creatinine
renal failure
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raised ferritin, raised ESR and CRP with mild microcytic anaemia
Inflammatory cause (cancer, rheumatoid arthiritis, TB. HIV, osteomyelitis, endocarditis
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what causes increased O2 dissociation from haem?
Increased temp and DPG, reduced pH
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types of haem in adult haem?
2 alpha, 2 delta
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what is the bohr affect?
lactic acid produced by anaerobic respiration reduces blood pH, increasing oxygen dissociation.
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what causes sickle cell?
recessivemutation in B globin gene turning glutamic acid into valine
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consequences of sickle cell?
haem structure collaplses. RBC becomes fibrous, insoluble and sticky, carrying less O2 and blocking vessels, causing tissue infarction.
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thalassaemia causes?
alpha: deletion/mutation in HBA1/2. four levels of condition. Beta: mutation/deletion in HBB gene
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in alpha thalassaemia, what do 3 mutation cause?
micro, hypo hameolytic anaemia and jaundice.
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red blood cells?
6-8 micrometers, about 5,000,000/microleter
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first degree heart block?
enhanced PR interval. block before/at AV node
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2nd heart block (m type 1)
PR interval increases until skipping. Blockage above/below His.
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2nd heart block (m type 2)
no elongation, sudden skipping. Blockage at His/purkinje. Need pacemaker
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3rd block.
extended QRS and P replaces R. ventricular pacemaker
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atrial flutter
few QRS complexes, sawtooth P waves.
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A fib
P waves irregular, QRS infequent. Atrial discharge at 300-600bpm
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Ventricular ectopic beats
His not conducting., v fib, wonky QRS complex.
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v fib
loss of effective v contraction. endless sawtoothing.
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order of septation in the developing heart?
at 4 weeks, partial septum forms AV canals. Primary septum separated atria, secondary septum forms foramen ovale. Aortic pul septum causes aorta and pul. artery to twist around each other.Atrio ventricular septum forms
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what is tetralogy of Fallot?
congenital pulmonary stenosis, overriding aorta, ventricular septal defect, right ventricular hypertrophy.
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what are the zones of the kidney and what do they produce
ZG: aldosterone. ZF: cortisol and androgens. ZR: cortisol and androgens. medulla: adrenaline
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what is Cushing's syndrome?
chronic excess cortisol caused by a pituitary tumour. Weight gain, moon face epidermis atrophy, hypertension, muscle weakness
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what are trisomies 13 and 18?
13: Patau's, 18: Edward's.
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what is reciprocal translocation?
two chromasomes 'swap ends'
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difference between nonsense and missense mutations?
nonsense: change in frame results in premature stop codon. Missense: change in one AA for another in the sequence.
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what diseases can a FGFR3 mutation cause?
Thanatophoric dysplasia, achondroplasia and hypochondroplasia
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what is the result of Haemophilia A+B mutations?
factors VIII and XI deficiency
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what is Lyon's hypothesis?
only one X gene is active at a time in one cell
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which follicle is arrested at prophase diplotene?
primordial follicle
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which follicle is arrested at metaphase II before puberty?
pre-ovulatory phase follicle
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what hormones are secreted from Paraventricular cells via anterior pituitary?
TSH, FSH, LH, prolactin, ACTH and GH
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what hormones are secreted from supraoptic via posterior pituitary?
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what hormones are secreted from magnocellular via posterior pituitary?
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what does the hypothalamus secrete to get anterior pituitary to release hormones?
TRH GnRH CRH GHRH Dopamine and Somatostatin
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what can happen to a Spermatogonium A up to 16 days after creation as part of the spermatogenic cycle?
Sudden arrest
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what is present in extracellular fluid in sertoli cells to aid sperm development?
Androgen binding protein and testosterone
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what are the WHO normal sperm statistics?
***** volume: 1.5ml. [sperm]: 15x10 6. total motility: 40%. progressive motility: 32%. normal morphology: 4%. vitality: 58%
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what is the window of fertility?
6 days: five days preovulation, one day ovulation.
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what is the period of human development?
38 weeks and two days
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what is parity?
the number of foetus' given birth above 24 weeks GA.
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what is capacitation?
sperm aquire ability to fertilise. Removal from sperm plasma membrane of glycoproteins and sterol groups.
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what is activation?
sperm 'whiplash' gaining motility. Plasma membrane breaks down to release hydrolyric enzymes (acrosome reaction).;
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describe the myometrium layers
two layers of longitudinal muscle sandwich a circular muscle layer
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what is high oestrogens effect on C. mucus?
thin, watery, high spinnbarkeit
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what is high progesterones effect on C. mucus?
thick and viscous.
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what is ectropion?
cervix rolls out after birth. simple columnar epithelium rolls out, exposed to bleeding and inflammation. undergoes metaplastic change over time.
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what glycoprotein does sperm bind to at the zona pellucida?
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in what layers are the muscle layers of the stomach from lumen outwards?
Oblique, circular, longitudinal
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what is the function of interstitial cells of Cajal?
intrinsic pacemaker generating slow wave impulses
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which spincters contract/relax spincters?
alpha: contract. beta: relax.
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somatostatin function?
reduces acid secretion (D cells)
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secretion function?
increases bicarbonate reduces acid (S cells)
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CCK function?
increase enzyme release and gall bladder contraction (I cells)
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what does H. Pylori secrete?
ammonia, cytotoxin associated gene A, vasculating cytotoxin A
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what innervates parotid gland?
glossopharyngeal nerve
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what innervates sublingual and submandibular glands
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what is given for alcohol withdrawal symptoms?
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when would you get Mallory body formation?
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what are Kaupffer cells?
phagocytes in the liver that destroy undigestible particles.
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what are stellate cells?
pericytes with immune function which absorb vit A and fat
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what is the gonadostat hypothesis of puberty?
reduced sensitivity to steroid hormone affect on the negative feedback on FSH/LH
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what is the maturation of CNS hypothesis of puberty?
GnRH neurones in pituitary mature, stimulated by achieving critical body weight (47kg girls, 55kg boys, 22%body weight). GnRH also stimulated by Leptin/Kissleptin
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which enzyme rises rapidly at the start of puberty?
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precious puberty?
maturation before age 8 or menstruation 10.
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what happens to the devleoping trachea at 7 weeks?
tracheooesophageal septum forms. Narrow lumen is recanalised.
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where does the pancreatic buds form from?
caudal foregute>duodenum>ventral/distal buds.
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what does the distal pancreas form on fusion?
rotates round to form uncinate process and distal head of pancreas
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two major types of bile acids and ratio?
glycine and taurine (3:1)
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important enzyme in bile acid synthesis?
7 alpha hydroxylase
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amount bile acid produced per day
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how is fat absorbed in the s intestine?
passively through Micelles or through CD34 channels
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what passes through the diaphragm at L8
Vena Cava, Pericardiophrenic nerve and right phrenic nerve
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what passes through the diaphragm at L10
Oesophagus, R/L phrenic nerve
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what passes through the diaphragm at L12
aorta, thoracic duct and azygous/hemizygous
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what enzyme in the endogenous pathway converts cholesterol and lecithin to cholesterol eesters and lysolecithin?
LCAT enzyme
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what enzyme in the endogenous pathway transfers cholesterol from HDL to LDL's?
CETP enzyme
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what transporter removes HDL from cells?
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what receptor on the liver does HDL bind to?
SR-B1 receptor
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what is the rate limiting step in lipid absorption?
the unstirred water layer
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what are the causes of lipid malabsorption?
Pancreatic insufficiency, bile acid deficiency, liver disease, gallstones, bacteria overgrowth, ileal disease, abetaliproproteinaemia and lymphatic deficiency
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what is Dovey's law?
blood flow=difference in aorta and vena cava pressure/resistance
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what is Poiseulle's law?
velocity=flow/cross sectional area
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What agonist does Novacure block and what receptor does it bind to?
Leukotriene D4 agonist on LTD4
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which routes of absorption avoid 1st pass metabolism?
rectal, sublingual, transdermal.
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what is Montelukast's dose, bioavailability and route of absorption?
10mg, 64% and oral.
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what factors affect drug absorption in the GI tract?
motility, size/formula, food interaction and pH (pH partitioning).
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what plasma protein binds acidic drugs?
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what plasma protein binds basic drugs?
acid glycoproteins/beta-globulins
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what does an extensive plasma protein binding do to drug action/elimination?
increases it.
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what rough Vd does total body water have?
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what rough Vd does extracellular fluid have?
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what rough Vd does plasma have?
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what rough Vd does fat have?
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what major vessels drain lymph from abdominal viscera?
mesenteric and inguinal back nodes into the Thoracic duct.
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where does lymph drain from the breast?
75% axillary nodes 25% parasternal nodes.
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what is phase 1 of 1st pass metabolism?
introduction/exposure of a functional group
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what is phase 2 of 1st pass metabolism?
attachment of a endogenous group to make it hydrophilic enough to excrete (gluconidaration).
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what enzyme group is involved with 75% of all drug metabolism?
Cytochrome P450's
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most gluconidarated drugs are inactive. what is the major exception?
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what enzymes aid gluconidaration
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in a paracetemol overdose, what is it converted to by hydroxylation?
NAPQI, which causes DNA and protein damage. Cannot be detoxified by GSH
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how do you treat a paracetemol overdose?
charcoal, N acetylcysteine (increases glutathione synthesis>GSH production)
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what factors cause greater bio availability?
liver failure, neonate lack of cytochromes, elderly and polymorphism.
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which alcohol related enzyme do 30-50% of east asians lack and is inhibited by antabuse?
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what toxic metabolite is paracetemol converted into during OD?
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how do you treat paracetemol overdose?
charcoal and N acetylcysteine
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what do alpha granules in clotting release?
vWf, fibrinogen coag factors and glycoproteins?
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what do beta granules release in clotting?
ATP/ADP serotonin
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glycoprotein that allows platelet direct binding to collagen?
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glycoprotein that allows platelet vW collagen binding?
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intrinsic clotting factors and measurement?
8,9,11,12, Activate partial thromboplastin time (APTT)
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extrinsic clotting factors and measurement?
7. Prothombin time (PT)
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vit k dependent clotting factors?
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what is the bainbridge affect?
reflexive tachycardia-selective increase in ach release to SNA, increasing HR but not vasoconstriction
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what is postural hypotension?
going from lying to standing, blood moves from middle to legs, causing reduction in arterial BP, causing body to undergo reflexive tachcardia to restore balance until venous pooling ends
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what is the limiting factor on cardiac output?
diastolic filling time
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what substances oppose coagulation?
prostacyclin, NO, Proteins S and C, antithombin.
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what is factor V Leiden?
mutation in factor V causes slowed deactivation by protein C, causing clotting tendency
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what converts plasminogen>plasmin to break down fibrin?
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which clotting factor do Haemophilia A sufferers lack?
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with what mechanisms does the body respond to shock?
ADH release and renin-angiotensin pathway to reduce fluid loss. sympathetic stimulation of glycogen breakdown to increase blood osmolality allowing autotransfusion. ACTH release increases.
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when is atrial naturetic peptide (ANP) released and what does it do?
released from heart during stretching. Increases vasodilation, inhibiting water reabsorption and renin/angiotensin.
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how do you define hypertension in the under 50's?
BP >150/90
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causes of secondary hypertension?
renal artery stenosis, aortic stenosis, hyperaldosteronism, phaeochromocytoma, meds, pregnancy and renal disease
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what should an arterial thrombus be treated with?
antiplatelet drugs
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what should a venous thrombus be treated with?
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where is heparin made and what does it do?
secretory granules of MAST cells. makes antithombin 1000x more active
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when would you use low molecular weight heparin?
in injected doses to counteract shortterm venous thromboembolism/risk
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how would you counterract a LMWH overdose?
IV prolamine.
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how does warfarin work?
reduces vit K reductase activity, preventing activation factors 2,8,9,10
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what is the recommended salt intake?
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what is APOB's function?
receptor recognition
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what is APOE's function?
structural ligand binding
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what is APOC's function?
activation/inhibition lipolysis
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what is APOa1's function?
cholesterol efflux
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what does APOE3 mutation cause?
hyperlipidaema and hypercholesteralaemia
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how do you treat hypercholesterolaemia?
statins, cholesterol absorption inhibitors, fibric acid derivatives, nicotinic and bile acids
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what occurs during isoosmotic dehydration?
reduced extracellular volume (nacl=water loss)
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what happens during hypoosmotic dehydration?
intracellular osmol reduces, vol increases. extracellular osmo reduces and volume decreases (NACL>water loss).
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what happens during hyperosmotic dehydration?
intra: increases osmol, reduced volume, Extra: osmo increases, volume decreases
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what does the macula densa release to reduce renal blood flow?
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how do NSAID's damage kidneys?
reduced perfusion of kidneys trigger prostaglandin release for vasodilation. NSAID's inhibit prostaglandins
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how is GFR calculated?
u[inulin] x V /[inulin]plasma
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at what rate is creatinine produced?
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haemoglobin levels (Hb)


men: 130-180g/L. women: 115-165g/L

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mean cell volume


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mean cell haemoglobin


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mean cell haemaglobin [..]


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