Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

ACS > Biochemistry > Flashcards

Biochemistry Flashcards

1
Q

urine output per day

A

1L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

GFR

A

glomerular filtrate both kidneys each minute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

sodium in the tubes

A

140 mmol at beginning and end

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

proximal tubule reclaims

A

100% bicarb, glucose, urate, AA
70% sodium, potassium, calcium, chlorine

HNaCl (Na and Cl back to blood, H into urine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

V max glucose

A

10mmol

blood glucose above this will cause glucose in urine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

potassium reabsorption pump

A

reabsorbes a large amount of K in proximal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

hypertonic medulla

A

1200-1400

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

loop of henle

A

countercurrent multiplication and countercurrent exchange

passive down
active up, lots of pumps. Diluts the urine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

normal range for ADH

A

doesn’t exist.

depens on plasma composition and body status.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

aldosterone works on:

A

distal tubule
NaKH pump
increases sodium reabsorption and K/H secretion
water follows passively.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

renin-angiotensin-aldosterone

A 
low pressure or sodium intake
renin
angiotensin 1
angiotensin 2 (thirst) (vasocontriction)
aldosterone
renal sodium and water retention
increased perfusion

angiotensin also causes vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

High potassium

A

can directly stimulate aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

high plasma osmolality

A 
hypothalamus (supra-optic and paraventricular n)
ADH
kidney increased water permeability
increased water ONLY reabsorption
decreased plasma osmolality.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

ADH triggered by

A

opiates
pain/nausea
decreased blood volume by 10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

surgery stimulates ADH

A

and causes water retention as a result.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

urea

A

is a rubbish test because protein breakdown is not constant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

creatinine

A

constant turn over
not regulated by enzymes
depends on muscle mass.

frail old people will have an misleadingly normal creatinine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

serum creatinine concentration

A

opposite of GFR

below GFR of 90- creatinine starts to soar!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

GFR=K/serum creatinine

A

K=creatinine production rate (estimate for each patient)

age and sex to estimate
muscle mass

needs to be adjusted for African

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

T3

A

5x more active- mostly from deionised T4 (in peripheries)

99% bound

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

T4

A

only thyroid- 99% bound to thyroid binding globulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

3 proteins which bind thyroid hormone

A

thyroid binding globulin
thyroid binding pre-albumin
albumin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

primary hypothyroidism

A

HIGH TSH
low FT4

thyroid not producing enough FT4
(FT3 doesn’t matter)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

compensated hypothyroidism

A

raised TSH
low/normal FT4
+ve antithyroid peroxidase antibodies

if they have antibodies you have to check every year

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

no FT4 measurable??

A

on thyroxine replacement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

over replacement of tyroxine

A

may cause AF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

thyroxine treatment

A

should be on for at least 6 weeks before checking or changing dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

primary hyperthyrdoism

A

undetectable TSH
high FT4
high FT3

producing adenoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

super raised FT3 with normal fT4

A

FT3 toxicosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

TSH suppressed by

A

IL-1+TNF (cytokines in illness)
Somatostatin
Glucocorticoids
Dopamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

anticonvulsants and thyroid

A

low FT4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

beta blockers and thyroid

A

hyperthyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

lithium and thyroid

A

hypothyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

amiodarone and thyroid

A

hyper and hypothyroidism (lots of iodine).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

hCG and pregnancy

A

stimulate TSHR
raised FT3/4
low TSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

raised/normal TSH and raised FT4?!

A

TSH secreting tumour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

secondary hypertension

A 
endocrine (aldosterone, phaeochromocytoma, Cushings,)
renal hypertension
hypertension in pregnancy
contraceptives
CoA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

mineralocorticoid hypertension

A 
aldosterone producing adenoma CONNS
bilateral hyperplasia
primary adrenal hyperplasia (unilateral)
aldosterone producing carcinoma
familial hyperaldosteronism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

screening for people with hypertension and hypokalaemia

A

plasma renin activity
plasma aldosterone concentration
- morning blood sample

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

testing for suspected CONNS

A

saline infusion test- should suppress aldosterone (as there is extra salt and water)
then
fludrocortisone suppression test- further sodium loading should lower plasma aldosterone

if both show no affect on aldosterone you know that you have primary hyperaldosteronism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

selective venous catheterization for a

A

aldosterone/cortisol ratio

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

phaeochromocytomas

A 
chromaffin tissue
sympathetic nervous tissue
adrenal medulla
most benign
MEN II and Von Hippel Landau
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

24 hour catecholamine urine

A

good for catching episodic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

blood catecholamines

A

short half life- so no good really.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

positive catecholamines in urine?

A

CT/MRI
MIBG
PET
plasma metanephrins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

pituitary hyperfunction

A

usually single hormone involved (PRL, GH, ACTH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

pituitary hypofunction

A

usually generalised.

tumours, infarction, surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

growth hormone stimulated by

A

stress, exercise, AA, sleep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Growth hormone inhibited by

A

glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

GH is an antagonist for

A

insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

GH and calcium

A

GH increases gut calcium absorptino

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

diagnose GH excess

A

basal GH and IGF1

GTT suppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

growth hormone deficiency

A

small children
doesn’t do much to adults

LAron (receptor defect)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

diagnosing GH deficiency

A 
STIMULATION
insluin
glucagon (kids under 5)
argining
clonidine

failure of two stimuli=deficient.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

causes of hyperprolactinaemia

A 
pregnancy
stress
dopamine antagonists
macroprolactin
pituitary tumour
pituitary stalk lesion
primary hypothyroidism
chronic renal failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

adrenal cortex

A

GFR- corisol from cortex
aldosterone from glomerulosa
catecholamines from medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

21 hydroxylase failure causes

A

increased androgens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

cortisol

A

blocks insulin
increases gluconeogenesis
immunosuppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

stress stimulates cortisol CRH

A 
cortisol from anterior pituitary
adrenal cortex
cortisol
low at night.
high in morning.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

primary adrenal insufficiency

A

congenital adrenal hyperplasia

enzyme defect- 21 hydroxylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

secondary adrenal insuffiencey

A

steroids (low ACTH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

adrenal insufficiency causes the following:

A

low glucose
low sodium
high potassium

low of water to correct hyponatraemia
hypotension
pigmentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

tests for addisons

A

serum cortisol
synachten test
(250micro IM cortisol–> absolute by >600 in an hour)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

CAH

A

increased 17 alpha OH progesterone (precursor)

low aldosterone
low cortisol

high testosterone
high oestradiol! makes sense now

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

undertreated CAH

A

rapid growth but short stature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

hypercortisolism

A 
pituitary cushing's disease (hight ACTH)
ectopic (lung tumour) (high ACTH)
adenoma (low ACTH)
carinoma (low ACTH)
iatrogenic (low ACTH)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

pseudo cushings

A

alcohol
obesity
depression

68
Q

investigating cushings

A

serum cortisol- midnight/08:00
salivary cortisol
urine free cortisol

best: dexamethason suppression
1mg over night. cortisol shoudl be <50 in morning

69
Q

Yanovski test

A

cushings

70
Q

bilateral inferior petrosal sinus sampling

A

to see if over production of ACTH from pituitary

71
Q

if no cause for high cortisol found?

A

consider chronic renal failure

72
Q

aki

A

nausea, malaise, confusion from retained nitrogenous waste
reduced GFR- volume overload
retain potassium

73
Q

life threatening potassium

A

> 8

tall tented t waves

74
Q

urea proportionate to protein intake

A

large bleed- large protein intake

75
Q

pre renal treatment

A

fluids

76
Q

renal AKI treatment

A

dialysis

77
Q

pre renal uraemia

A

urine more than 2x plasma concentration

urinary sodium less than 15

78
Q

ATN

A

urine: plasma osmo the same

urinary sodium more than 40

79
Q

stage 1 renal impairment

A

> 90

80
Q

stage 2 renal impairment

A

60-90

81
Q

stage 3 renal impairment

A

30-60
hypertension
low calcium causes–>
secondary hyperparathyroidism

82
Q

stage 4 renal impairment

A

15-30
anaemia
anorexia
high phosphate

83
Q

stage 5 renal impairment

A

<15
acidosis
hyperkalaemia

84
Q

chronic renal failure and electrolytes

A 
high urea/Cr
acid
high K
low Ca
reduced vit D hydroxylation
reduced Epo (anaemia)
increased cholesterol and TG
impaired immune
85
Q

glomerular damage

A

oliguria (water can’t get in)

86
Q

tubular damage

A

polyuria (water can’t get back out)

87
Q

low vit D in CKD

A 
low vit D
low calcium absorption from gut
low plasma calcium
high parathyroid (osetitis fibrosa- high bone resorption)
osteomalacia
88
Q

bones in CKD

A

osteomalacia- low calcium
osteitis fibrosa- high PTH

metastatic calcification- high calcium:phosphate product
bone decay- porosis: dissolved bone buffers in acidosis

89
Q

hypophosphataemic ricketts

A

tubular disorder

90
Q

type 1 renal tubular acidosis

A

distal
fails to secrete H- acidosis
excess K loss (low K)
TREAT WITH BICARB AND K

91
Q

type 2 rental tubular acidosis

A

proximal
bicarb leak
TREAT with bicarb

92
Q

type 4 renal tubular acidosis

A

low renin and aldosterone

high potassium because can’t excrete H and K

93
Q

acid base balance

A

the regulation of hydrogen ions

94
Q

CO2+H2O

A

H2CO2

95
Q

acids produced by the body

A 
carbonic
hydrochloric
lactic
keto
uric
proteins
96
Q

bases produced by the body

A

bicarb
phosphate
proteins
ammonia

97
Q

Buffers

A 
BICARB
haemoglobin
proteins
phosphate
ammonia
98
Q

Hb as a buffer

A

CO2 loss in alveoli

99
Q

pH=

A

HCO3- / pCO2

100
Q

physiological compensation for metabolic acidosis

A

vomiting
hyperventilation
renal H+ loss

101
Q

where in kidney is bicarb reabsorbed?

A

proximal tubule
add a H to make H2CO3
CO2 leaves and water left in tubule

102
Q

phosphate in kidney

A

picks up a hydrogen at the proximal tubule and excretes dihyrdogen phosphate in urine

103
Q

metabolic acidosis

A 
ketoacidosis
diabetic or alcoholic lactic acidosis
hypoxia
poisonins
acid ingestion
renal failure- can't clear H+
loss of bicarb- dairrhoea, renal tubular acidosis
104
Q

metabolic alkalosis

A 
almost always due to volume contraction
vomiting
diuretics
profound hypokalaemia
renal failure
hyperaldosteronism
XS alkali from docs
105
Q

respiratory acidosis

A 
lung disease
trauma
myopathies
pneumothorax
CNS depression
106
Q

respiratory alkalosis

A 
excessive ventilation on ITU
anaemia
altitude
central neuro
voluntary, psychogenic
ANXIETY
107
Q

anion gap range

A

normal is 12 =-2

108
Q

increased anion gap

A

renal failure
ketoacidosis
lactic acidosis
intoxication (aspirin, metformin)

109
Q

decreased anion gap

A

low protein
multiple myeloma
lithium

110
Q

acidaemia and potassium

A

acidaemia produces hyperkalaemia

111
Q

low chloride means…

A

alkalosis

112
Q

obligate water loss

A

500 skin
500 kidneys
400 lungs
100 gut

=1500 a day

113
Q

glucose and sodium

A

hyperglycaemia causes a compensatory hyponatraemia (osmotic)

114
Q

SIADH

A

cancers (lung, pancreas, lymphoma)
pulmonary disorders (pneumonia, bronchiectasis etc)
neurological disorders- damage pituitary/hypothalamus

115
Q

what type of saline in an emergency

A

hypertonic!

avoid cerebral oedema

116
Q

causes of hypernatraemia

A

inadequate water intake
impaired water retention
loss of hypotonic fluids

excess sodium intake
increased sodium retention (CONNS)

117
Q

Diabetes insipidus test

A

water deprivation
if osmolarity increases then it is cranial
if osmolarity is the same then it is nephrogenic

118
Q

treatment for cranial DI

A

desmopressin

119
Q

treatment for nephrogenic DI

A

drink lots!

thiazides

120
Q

LDL=

A

Total cholesterol-Highdenisity /2.2

121
Q

Non-HDL=

A

total cholesterol-HDL

122
Q

all types of lipoproteins contain same fat but different

A

transport mediums

123
Q

IDL

A

only really in type 3 hyperlipidaemia

124
Q

chylomicron

A

normal after meal
not normal in fasting state

type 1 hyperlipidiaemia

125
Q

cholesterol and CHD risk

A

total cholesterol-increase risk
triglycerides-increase risk
HDL- inverse risk

126
Q

causes of high lipids

A 
diabetes
liver
hypothyroidism
alcohol
renal failure
HIV
anorexia
127
Q

familial hypercholesterolaemia

A

cholesterol above 7.5
LDL receptor defect
STATINS

128
Q

familial combined hyperlipidaemia

A

cholesterol 5-10mmol/L
too much VLDL by liver
STATINS

129
Q

type 3 hyperlipidaemia

A

alcohol
poor diet
cholesterol 5-15
STATINS FIBRATES

130
Q

hypertriglyceridaemia

A

lipo-protein deficiency

FIBRATES

131
Q

statins

A

HMGCoA reductor inhibitor

good for cholesterol!

132
Q

fibrates

A

good for TG

but myositis and LFTs

133
Q

fish oil omacor

A

decrease triglycerides

134
Q

parathyroid hormone

A

stimulated by low calcium, low magnesium and high vit D.

135
Q

net effect PTH

A

increase calcium

decreased phosphate

136
Q

insulin actions

A

increase muscle uptake of glucose
increase glycogen syntehsis in liver
inhibit fat breakdown
increase fat synthesis

137
Q

glucacon…

A

increase liver GNG

138
Q

adrenalin…

A

increase glucoLYSIS increase lipoLYSIS

139
Q

growth hormone…

A

increase protein synthesis

decrease utilization of glucose

140
Q

cortisol and glucose

A

decrease glucose uptake

increase GNG

141
Q

HbA1c

A

percent of haemoglobin
glycation of N terminal valine of Hb beta chains
last 2-3 months

142
Q

microalbuminuria risk factor for

A

nephropathy
CVD
total mortality

reversible!

143
Q

somogyi effect

A

to do with blood glucose during the day

144
Q

non-islet cell tumours

A

rare mesenchymal tumours
sarcoma, hepatoma
release IGF1 or 2
poor prognosis

145
Q

primary ovarian failure

A

high LH/ VERY HIGH FSH
(can’t produce follicles)
impaired follicular development

146
Q

secondary ovarian failure

A

low LH and FSH
impaired LH/FSH production

due to prolactinoma
hypopituitarism

147
Q

testicular failure

A

hypergonadotrphic hypogonadism

148
Q

urine potassium excretion depends on

A

availability of sodium for exchange
aldosterone
relative intracellular potassium and hydrogen

149
Q

loop diuretics

A

block Na reabsorption in proximal tubule
lots of Na left at distal tubule
so lots of K lost

150
Q

potassium pump also affected by

A

insulin and catecholamines

after MI may get hypokalaemia
sudden refeeding may cause huge shift back into cell

151
Q

treatment hyperkalaemia

A

calcium gluconate- antagonise
salbutamol
insulin
naHCo3

152
Q

Sando K for

A

hypokalaemia

153
Q

AST/ALT

A

transanimases

intracellular
liver damage

also increased in pancreatitis and haemolysis
increase in MI and skeletal muscle diseae

154
Q

ALP

A

cholestasis

in OB and liver surface

raised in bone disease (Paget’s) and cholestasis
raised in hepatitis and osteomalacia etc.

155
Q

raised gamma GT in

A

cholestasis and hepato cellular damage

156
Q

CK M/B

A

very raised in polymyositis, rhabdomyolysisis and duechennes

raised in trauma, surgery, mysositis

slightly raised with statins, hypothyroidism and Africans

157
Q

TnT, TnI

A

4-6 hours post MI

158
Q

Amylase

A

very raised in acute pancreatitis, DKA, renal failure

raised in abdo problems, salivary problems, morphine

159
Q

CA153

A

breast cancer

160
Q

low albumin causese

A

oedema
decrease calcium binding
altered drug activity
kernicertus in babies!

161
Q

neonates and albumin

A

its low!

162
Q

CRP

A

injury, inflammation, infection

163
Q

alpha 1 anti tripson

A

inhibits protease
COPD, emphysema
liver disease

164
Q

polyclonal gammaglobulinopathy

A

infection
liver
autoimmune

165
Q

monyclonal gammaglobulinopathy

A

multiple myeloma
MGUS
Waldenstrom

166
Q

detectable urine albumin level

A

> 300mg

ACS (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions