Biochemistry Flashcards
1
Q
urine output per day
A
1L
2
Q
GFR
A
glomerular filtrate both kidneys each minute
3
Q
sodium in the tubes
A
140 mmol at beginning and end
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)
5
Q
V max glucose
A
10mmol
blood glucose above this will cause glucose in urine.
6
Q
potassium reabsorption pump
A
reabsorbes a large amount of K in proximal
7
Q
hypertonic medulla
A
1200-1400
8
Q
loop of henle
A
countercurrent multiplication and countercurrent exchange
passive down
active up, lots of pumps. Diluts the urine.
9
Q
normal range for ADH
A
doesn’t exist.
depens on plasma composition and body status.
10
Q
aldosterone works on:
A
distal tubule
NaKH pump
increases sodium reabsorption and K/H secretion
water follows passively.
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
12
Q
High potassium
A
can directly stimulate aldosterone
13
Q
high plasma osmolality
A
hypothalamus (supra-optic and paraventricular n) ADH kidney increased water permeability increased water ONLY reabsorption decreased plasma osmolality.
14
Q
ADH triggered by
A
opiates
pain/nausea
decreased blood volume by 10%
15
Q
surgery stimulates ADH
A
and causes water retention as a result.
16
Q
urea
A
is a rubbish test because protein breakdown is not constant
17
Q
creatinine
A
constant turn over
not regulated by enzymes
depends on muscle mass.
frail old people will have an misleadingly normal creatinine.
18
Q
serum creatinine concentration
A
opposite of GFR
below GFR of 90- creatinine starts to soar!
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
20
Q
T3
A
5x more active- mostly from deionised T4 (in peripheries)
99% bound
21
Q
T4
A
only thyroid- 99% bound to thyroid binding globulin
22
Q
3 proteins which bind thyroid hormone
A
thyroid binding globulin
thyroid binding pre-albumin
albumin
23
Q
primary hypothyroidism
A
HIGH TSH
low FT4
thyroid not producing enough FT4
(FT3 doesn’t matter)
24
Q
compensated hypothyroidism
A
raised TSH
low/normal FT4
+ve antithyroid peroxidase antibodies
if they have antibodies you have to check every year
25
no FT4 measurable??
on thyroxine replacement
26
over replacement of tyroxine
may cause AF
27
thyroxine treatment
should be on for at least 6 weeks before checking or changing dose
28
primary hyperthyrdoism
undetectable TSH
high FT4
high FT3
producing adenoma
29
super raised FT3 with normal fT4
FT3 toxicosis
30
TSH suppressed by
IL-1+TNF (cytokines in illness)
Somatostatin
Glucocorticoids
Dopamine
31
anticonvulsants and thyroid
low FT4
32
beta blockers and thyroid
hyperthyroidism
33
lithium and thyroid
hypothyroidism
34
amiodarone and thyroid
hyper and hypothyroidism (lots of iodine).
35
hCG and pregnancy
stimulate TSHR
raised FT3/4
low TSH
36
raised/normal TSH and raised FT4?!
TSH secreting tumour
37
secondary hypertension
```
endocrine (aldosterone, phaeochromocytoma, Cushings,)
renal hypertension
hypertension in pregnancy
contraceptives
CoA
```
38
mineralocorticoid hypertension
```
aldosterone producing adenoma CONNS
bilateral hyperplasia
primary adrenal hyperplasia (unilateral)
aldosterone producing carcinoma
familial hyperaldosteronism
```
39
screening for people with hypertension and hypokalaemia
plasma renin activity
plasma aldosterone concentration
- morning blood sample
40
testing for suspected CONNS
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
41
selective venous catheterization for a
aldosterone/cortisol ratio
42
phaeochromocytomas
```
chromaffin tissue
sympathetic nervous tissue
adrenal medulla
most benign
MEN II and Von Hippel Landau
```
43
24 hour catecholamine urine
good for catching episodic
44
blood catecholamines
short half life- so no good really.
45
positive catecholamines in urine?
CT/MRI
MIBG
PET
plasma metanephrins
46
pituitary hyperfunction
usually single hormone involved (PRL, GH, ACTH)
47
pituitary hypofunction
usually generalised.
| tumours, infarction, surgery
48
growth hormone stimulated by
stress, exercise, AA, sleep
49
Growth hormone inhibited by
glucose
50
GH is an antagonist for
insulin
51
GH and calcium
GH increases gut calcium absorptino
52
diagnose GH excess
basal GH and IGF1
| GTT suppression
53
growth hormone deficiency
small children
doesn't do much to adults
LAron (receptor defect)
54
diagnosing GH deficiency
```
STIMULATION
insluin
glucagon (kids under 5)
argining
clonidine
```
failure of two stimuli=deficient.
55
causes of hyperprolactinaemia
```
pregnancy
stress
dopamine antagonists
macroprolactin
pituitary tumour
pituitary stalk lesion
primary hypothyroidism
chronic renal failure
```
56
adrenal cortex
GFR- corisol from cortex
aldosterone from glomerulosa
catecholamines from medulla
57
21 hydroxylase failure causes
increased androgens
58
cortisol
blocks insulin
increases gluconeogenesis
immunosuppression
59
stress stimulates cortisol CRH
```
cortisol from anterior pituitary
adrenal cortex
cortisol
low at night.
high in morning.
```
60
primary adrenal insufficiency
congenital adrenal hyperplasia
| enzyme defect- 21 hydroxylase
61
secondary adrenal insuffiencey
steroids (low ACTH)
62
adrenal insufficiency causes the following:
low glucose
low sodium
high potassium
low of water to correct hyponatraemia
hypotension
pigmentation
63
tests for addisons
serum cortisol
synachten test
(250micro IM cortisol--> absolute by >600 in an hour)
64
CAH
increased 17 alpha OH progesterone (precursor)
low aldosterone
low cortisol
high testosterone
high oestradiol! makes sense now
65
undertreated CAH
rapid growth but short stature
66
hypercortisolism
```
pituitary cushing's disease (hight ACTH)
ectopic (lung tumour) (high ACTH)
adenoma (low ACTH)
carinoma (low ACTH)
iatrogenic (low ACTH)
```
67
pseudo cushings
alcohol
obesity
depression
68
investigating cushings
serum cortisol- midnight/08:00
salivary cortisol
urine free cortisol
best: dexamethason suppression
1mg over night. cortisol shoudl be <50 in morning
69
Yanovski test
cushings
70
bilateral inferior petrosal sinus sampling
to see if over production of ACTH from pituitary
71
if no cause for high cortisol found?
consider chronic renal failure
72
aki
nausea, malaise, confusion from retained nitrogenous waste
reduced GFR- volume overload
retain potassium
73
life threatening potassium
>8
| tall tented t waves
74
urea proportionate to protein intake
large bleed- large protein intake
75
pre renal treatment
fluids
76
renal AKI treatment
dialysis
77
pre renal uraemia
urine more than 2x plasma concentration
| urinary sodium less than 15
78
ATN
urine: plasma osmo the same
| urinary sodium more than 40
79
stage 1 renal impairment
>90
80
stage 2 renal impairment
60-90
81
stage 3 renal impairment
30-60
hypertension
low calcium causes-->
secondary hyperparathyroidism
82
stage 4 renal impairment
15-30
anaemia
anorexia
high phosphate
83
stage 5 renal impairment
<15
acidosis
hyperkalaemia
84
chronic renal failure and electrolytes
```
high urea/Cr
acid
high K
low Ca
reduced vit D hydroxylation
reduced Epo (anaemia)
increased cholesterol and TG
impaired immune
```
85
glomerular damage
oliguria (water can't get in)
86
tubular damage
polyuria (water can't get back out)
87
low vit D in CKD
```
low vit D
low calcium absorption from gut
low plasma calcium
high parathyroid (osetitis fibrosa- high bone resorption)
osteomalacia
```
88
bones in CKD
osteomalacia- low calcium
osteitis fibrosa- high PTH
metastatic calcification- high calcium:phosphate product
bone decay- porosis: dissolved bone buffers in acidosis
89
hypophosphataemic ricketts
tubular disorder
90
type 1 renal tubular acidosis
distal
fails to secrete H- acidosis
excess K loss (low K)
TREAT WITH BICARB AND K
91
type 2 rental tubular acidosis
proximal
bicarb leak
TREAT with bicarb
92
type 4 renal tubular acidosis
low renin and aldosterone
| high potassium because can't excrete H and K
93
acid base balance
the regulation of hydrogen ions
94
CO2+H2O
H2CO2
95
acids produced by the body
```
carbonic
hydrochloric
lactic
keto
uric
proteins
```
96
bases produced by the body
bicarb
phosphate
proteins
ammonia
97
Buffers
```
BICARB
haemoglobin
proteins
phosphate
ammonia
```
98
Hb as a buffer
CO2 loss in alveoli
99
pH=
HCO3- / pCO2
100
physiological compensation for metabolic acidosis
vomiting
hyperventilation
renal H+ loss
101
where in kidney is bicarb reabsorbed?
proximal tubule
add a H to make H2CO3
CO2 leaves and water left in tubule
102
phosphate in kidney
picks up a hydrogen at the proximal tubule and excretes dihyrdogen phosphate in urine
103
metabolic acidosis
```
ketoacidosis
diabetic or alcoholic lactic acidosis
hypoxia
poisonins
acid ingestion
renal failure- can't clear H+
loss of bicarb- dairrhoea, renal tubular acidosis
```
104
metabolic alkalosis
```
almost always due to volume contraction
vomiting
diuretics
profound hypokalaemia
renal failure
hyperaldosteronism
XS alkali from docs
```
105
respiratory acidosis
```
lung disease
trauma
myopathies
pneumothorax
CNS depression
```
106
respiratory alkalosis
```
excessive ventilation on ITU
anaemia
altitude
central neuro
voluntary, psychogenic
ANXIETY
```
107
anion gap range
normal is 12 =-2
108
increased anion gap
renal failure
ketoacidosis
lactic acidosis
intoxication (aspirin, metformin)
109
decreased anion gap
low protein
multiple myeloma
lithium
110
acidaemia and potassium
acidaemia produces hyperkalaemia
111
low chloride means...
alkalosis
112
obligate water loss
500 skin
500 kidneys
400 lungs
100 gut
=1500 a day
113
glucose and sodium
hyperglycaemia causes a compensatory hyponatraemia (osmotic)
114
SIADH
cancers (lung, pancreas, lymphoma)
pulmonary disorders (pneumonia, bronchiectasis etc)
neurological disorders- damage pituitary/hypothalamus
115
what type of saline in an emergency
hypertonic!
| avoid cerebral oedema
116
causes of hypernatraemia
inadequate water intake
impaired water retention
loss of hypotonic fluids
excess sodium intake
increased sodium retention (CONNS)
117
Diabetes insipidus test
water deprivation
if osmolarity increases then it is cranial
if osmolarity is the same then it is nephrogenic
118
treatment for cranial DI
desmopressin
119
treatment for nephrogenic DI
drink lots!
| thiazides
120
LDL=
Total cholesterol-Highdenisity /2.2
121
Non-HDL=
total cholesterol-HDL
122
all types of lipoproteins contain same fat but different
transport mediums
123
IDL
only really in type 3 hyperlipidaemia
124
chylomicron
normal after meal
not normal in fasting state
type 1 hyperlipidiaemia
125
cholesterol and CHD risk
total cholesterol-increase risk
triglycerides-increase risk
HDL- inverse risk
126
causes of high lipids
```
diabetes
liver
hypothyroidism
alcohol
renal failure
HIV
anorexia
```
127
familial hypercholesterolaemia
cholesterol above 7.5
LDL receptor defect
STATINS
128
familial combined hyperlipidaemia
cholesterol 5-10mmol/L
too much VLDL by liver
STATINS
129
type 3 hyperlipidaemia
alcohol
poor diet
cholesterol 5-15
STATINS FIBRATES
130
hypertriglyceridaemia
lipo-protein deficiency
| FIBRATES
131
statins
HMGCoA reductor inhibitor
| good for cholesterol!
132
fibrates
good for TG
| but myositis and LFTs
133
fish oil omacor
decrease triglycerides
134
parathyroid hormone
stimulated by low calcium, low magnesium and high vit D.
135
net effect PTH
increase calcium
| decreased phosphate
136
insulin actions
increase muscle uptake of glucose
increase glycogen syntehsis in liver
inhibit fat breakdown
increase fat synthesis
137
glucacon...
increase liver GNG
138
adrenalin...
increase glucoLYSIS increase lipoLYSIS
139
growth hormone...
increase protein synthesis
| decrease utilization of glucose
140
cortisol and glucose
decrease glucose uptake
| increase GNG
141
HbA1c
percent of haemoglobin
glycation of N terminal valine of Hb beta chains
last 2-3 months
142
microalbuminuria risk factor for
nephropathy
CVD
total mortality
reversible!
143
somogyi effect
to do with blood glucose during the day
144
non-islet cell tumours
rare mesenchymal tumours
sarcoma, hepatoma
release IGF1 or 2
poor prognosis
145
primary ovarian failure
high LH/ VERY HIGH FSH
(can't produce follicles)
impaired follicular development
146
secondary ovarian failure
low LH and FSH
impaired LH/FSH production
due to prolactinoma
hypopituitarism
147
testicular failure
hypergonadotrphic hypogonadism
148
urine potassium excretion depends on
availability of sodium for exchange
aldosterone
relative intracellular potassium and hydrogen
149
loop diuretics
block Na reabsorption in proximal tubule
lots of Na left at distal tubule
so lots of K lost
150
potassium pump also affected by
insulin and catecholamines
after MI may get hypokalaemia
sudden refeeding may cause huge shift back into cell
151
treatment hyperkalaemia
calcium gluconate- antagonise
salbutamol
insulin
naHCo3
152
Sando K for
hypokalaemia
153
AST/ALT
transanimases
intracellular
liver damage
also increased in pancreatitis and haemolysis
increase in MI and skeletal muscle diseae
154
ALP
cholestasis
in OB and liver surface
raised in bone disease (Paget's) and cholestasis
raised in hepatitis and osteomalacia etc.
155
raised gamma GT in
cholestasis and hepato cellular damage
156
CK M/B
very raised in polymyositis, rhabdomyolysisis and duechennes
raised in trauma, surgery, mysositis
slightly raised with statins, hypothyroidism and Africans
157
TnT, TnI
4-6 hours post MI
158
Amylase
very raised in acute pancreatitis, DKA, renal failure
raised in abdo problems, salivary problems, morphine
159
CA153
breast cancer
160
low albumin causese
oedema
decrease calcium binding
altered drug activity
kernicertus in babies!
161
neonates and albumin
its low!
162
CRP
injury, inflammation, infection
163
alpha 1 anti tripson
inhibits protease
COPD, emphysema
liver disease
164
polyclonal gammaglobulinopathy
infection
liver
autoimmune
165
monyclonal gammaglobulinopathy
multiple myeloma
MGUS
Waldenstrom
166
detectable urine albumin level
>300mg
