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Case of crash Dieter Flashcards

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1
Q

lipoproteins?

A

lipid with amphipathic molecules surrounding (phospholipids) and apoliproteins so can float around in plasma

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2
Q

Classes of Lipoprotein?

A

chylomicron
VLDL
IDL
LDL
HDL

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3
Q

A1/2 role?

A

transfer of cholesterol from periphery to liver

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4
Q

endogenous lipid cycle in fasting ?

A

liver produces VLDL, which is broken down by lipoprotein lipase into free fatty acids and glycerol so IDL. then free fatty acids stored into fat tissue and the IDL is back in liver to be disposed of or moved into LDL to peripheral tissues

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5
Q

endogenous lipid cycle in fasting ?

A

liver produces VLDL, which is broken down by lipoprotein lipase into free fatty acids and glycerol so IDL. then free fatty acids stored into fat tissue and the IDL is back in liver to be disposed of or moved into LDL to peripheral tissues

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6
Q

role of the liver in endogenous?

A

triglyceride synthesis
export as VLDL
take up particles when triglyceride removed
LDL delivers cholesterol to peripheral cells

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7
Q

cholestrol is produced from?

A

acetate converted by HMG- CoA reductase

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8
Q

statins inhibit?

A

HMG coA reductase

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9
Q

when free cholesterol is low in cell?

A

N-SREBP transcription factor is switched on and the LDL receptor gene codes for LDL receptor protein

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10
Q

endogenous pathway, HDL particles produced from liver, what do they do?

A

absorb cholesterol from cells in the vascular endothelium and recycle it back to liver as LDL

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11
Q

exogenous pathway?

A

from dietary lipids- chylomicron particle are absorbed and broken down by lipoprotein lipase into free fatty acids and glycerol which then stored in adipose tissue

the remaining chylomicron is transported to liver

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12
Q

cholesterol and fatty acid in the gut are?

A

absorbed into intestinal mucosa cells and the reesterified to cholestrol ester and triglyceride and packaged with phospholipids and lipoproteins. they are then secreted into lymphatic vessels as chylomicrons

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13
Q

what happens to glycerol?

A

it is processed in liver to form more triglycerides or converted to glucose

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14
Q

what happens to the chylomicron remenant?

A

taken up by LDL receptors in liver

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15
Q

hepatic lipase features?

A

no cofactor,
substrate is IDL, HDL and LDL
present in liver, adrenal and endocrine

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16
Q

lipoprotein lipase features?

A

cofactor- ApoCII
substrate- CM and VLDL
tissues- adipose and skeletal muscle
regulation in feeding fasting and exercise

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17
Q

normal serum lipid concentration?

A

should be less than 5mmol/L

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18
Q

upper limit of normality for fasting triglycerides?

A

1.7mmol/L

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19
Q

HDL levels

A

above 0.9 mmol/l in men and 1.2 mmol/l

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20
Q

FH?

A

autosomal dominant disorder of lipid metabolism, usually hetereogenous
occurs in 1 in 270 people, raised cholestrol specifically LDL cholestrol

tendon and skin xanthomata

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21
Q

pathognomic for hypercholesterolaemia?

A

corneal arcus before age of 40

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22
Q

mutations of FH found?

A

ApoB
PCSK9
LDLR

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23
Q

causes of hypertriglyceridaemia?

A

obesity, DM, excess alcohol, renal failure, gout, drug treatment, thiazides, beta blockersm retinoic acid derivatives, oestrogen therapy

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24
Q

causes of hypercholestrolemia?

A

hypothyroidism, nephrotic syndrome, high saturated fat diet, cholestatic liver disease, anorexia nervosa

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25
obesity?
over 30
26
normal weight?
18.5-24.9
27
as obesity increases so does?
insulin resisitance
28
metabolic/ X syndrome?
reduced glucose tolerance, hyperinsulinaemia, hypertension, visceral obesity, homeostatic disorder, lipid disorder (high triglycerides, low HDL, normal or elevated LDL)
29
clinical identification metabolic syndrome
waist circumference: men> 94cm women> 80 cm plus any 2 of fasting triglycerides over 1.7 HDL men less than 1.03 women less than 1.29 blood pressure over 130/85 fasting glucose over 5.6
30
dying of cardiovascular disease in UK?
1: 3
31
Q Risk score?
age, cholestrerol, RA, renal, AF, sex, smoking status, FH, BMI, systolic blood pressure, left ventricular hypertrophy, T2DM
32
PCSK inhibitors?
block PCSK 9 protein which is responsible for degrading cholesterol receptors thus preventing removal of LDL from blood
33
Metabolic adaptation?
decreased energy expenditure, decreased satiety, improving metabolic efficiency, increased cues for energy intake
34
the only appetite inducing (orexigenic) hormone is?
ghrelin
35
ghrelin acts on?
NPY and AgRP neurons
36
what stimulates brain feeding?
accelerator neurons produce NPY
37
What causes inhibition of eating?
melanocortin peptides (brake)
38
acclerator and brake neurons work on?
arcuate nucleus
39
NPY neurons also?
produce agouti related peptides which block neuronal melanocortical receptors
40
ghrelin rises when?
stomach is empty, stimulates hunger neurons
41
PYY?
released before nutrients arrive in lower small intestine and colon and then a bit more, decreases food intake by inhibiting gut motility
41
PYY?
released before nutrients arrive in lower small intestine and colon and then a bit more, decreases food intake by inhibiting gut motility
42
GLP1?
secreted by EEC- l cells and certain neurons in the nucleus of the solitary tract in the brainstem. in response to food consumption glucose dependent insulinotropic peptide (GIP) is co secreted enhances insulin secretion
43
leptin is secreted by?
white adipose tissue
44
leptin interacts with?
mesolimbic dopamine system (motivation/reward) nucleus of solitary tract (satiety)
45
what happens in low energy diet?
increased hunger/desire reduction in PYY, cholecystokinin, insulin leptin and amylin ghrelin, GIP and pancreatic polypeptide increased?
46
how does exercise affect food?
increase in PYY levels so less appetite and ghrelin
47
in people with obesity?
intestinal enteroendocrine cell responsiveness is reduces blunted ghrelin reduction post meal reduced baseline and meal stimulated levels of anorectic peptides NT, GLP1 and PYY leptin resistance
48
drugs associated with?
antipsychotics: lithium, risperidone, quetiapine, apiprazole, olanzapine, valproic acid antidepressant: citalopram, duloxetine, venlafaxine sleep inducing agents: zopiclone, trazadone, zolpidem neuropathic- pregabalin/ gabapentin steroids insuline
49
anti- obesity agents?
CNS stimulants: phentermine, benzaphetamine, lorcaserin antidepressant/ dopamine reuptake inhibitor, opiod antagonist- naloxone, bupropion orlistat GLP1 RA metformin amylin agonists SGLT2 inhibitors
50
weight loss surgery requirements?
BMI over 40 between 35 and 39.9 with severe obesity related comorbidity between 30 and 34.9 and poorly controlled diabetes
51
weight loss surgery requirements?
BMI over 40 between 35 and 39.9 with severe obesity related comorbidity between 30 and 34.9 and poorly controlled diabetes
52
hind gut hypothesis?
glycaemic improvement is due to accelerated nutrient delivery to distal intestines GLP1 main contributor
53
likert scales?
unipolar (neutral/nothing to one extreme) or bipolar (negative extreme to positive extreme)
54
statistical test choice?
difference or correlation/association independent vs repeated parametric (meets normal distribution) vs non parametric
55
when comparing groups what test do you use?
2 groups- t test more than 2 groups - ANOVA compare the means
56
when testing association in a categorical or binary data then you use?
chi-square test
57
sertraline can cause?
low sodium/ GI bleeds
58
prochlorperazine can cause?
parkinsonism
59
why do you avoid giving ldopa at meal times?
it completes with meals
60
how to give bisphosphonates?
take on empty stomach, sitting up 30 mins before food
61
changes in elderly that will affect drug distribution?
decreased muscle mass increased body fat decreased serum albumin
62
why does low muscle mass affect drug distribution?
less volume of distribution for drugs that distribute into muscles, therefore greater plasma concentration e.g digoxin
63
digoxin toxicity?
bradycardia, junctional tachycardia, heart block, delirium confusion dizziness, anorexia, abdominal pain, green yellow vision double vision, photophobia
64
why is increased body fat bad?
increased volume of distribution of fat soluble drugs, therefore increased t1/2 e.g diazepam
65
side effects of benzodiazepines?
drowsiness, confusion, ataxia and dependency
66
treatment reversa for benzodiazepine?
iv flumazenil 200mcg
67
why is serum albumin important?
decreased albumin 12-25%- can reduce drug binding capacity and therefore more free drugi.e phenytoin/warfarin albumin could be further depressed by heart failure, renal disease, RA, hepatic cirrhosis and some malignancies
68
phenytoin toxicity?
CHANNT coarse facies hepatitis ataxia nystagmus nausea vomiting tremor
69
what can cause bleeding?
warfarin has a small volume of distribution, 99% bound asprin can replace, and a 1-2% displacement can double warfarin or triple concentration of free
70
adverse effects of antiplatelets (aspirin)?
renal failure fluid retention peptic ulcer disease bleeding tendency
71
how quick does GFR decline?
1% per year from age of 40
72
which drugs may be increased due to renal function reduction?
morphine, lithium
73
early toxicity lithium 1.5 mmol/L?
agitation, tremor, twitching
74
late toxicity lithium> 2 mmol/l?
fits, arrhythmia, renal failure
75
morphine undergoes?
phase 2 metabolism by conjugation, renal impariemnt leads to build up of metabolite
76
morphine toxicity?
DR CHAN drowsiness respiratory depression constipation hypotension and nausea vomiting
77
treatment for morphine?
iv naloxone 400 mcg
78
what pharmacodynamic effect on heart of elderly person?
reduced and delayed bronchodilatory response to b agonist decreased calcium channel block effect on PR interval
79
prescribing cascade?
medicines are being prescribed to treat side effects of other medicine
80
side effects of ACE i i.e ramipril?
dry cough hypotension potassium increase renal failure
81
calcium channel blockers side effects e.g amlodipine?
hypotension negatively inotropic fluid retention, facial swelling, ankle swelling
82
diuretics side effects?
hypotension hypokalaemia hyponatraemia confusion dehydration

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