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Case 10 Flashcards

1
Q

Which hormones are preferred in endocrine disorder tx and why ?

A

Exogenous options; recombinant or synthetic hormones are preferred due to the lower contamination risk

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2
Q

What is the MOA of insulin ?

A

Receptor binding causes phosphorylation of insulin responsive elements to ^ glucose traffic into cells via GLUT activity and ^ glycogen synthesis.

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3
Q

How would you treat an OD on insulin ?

A

Px is hypoglycaemic so tx with glucose and glucagon

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4
Q

What group of drugs are contraindicated on insulin and why ?

A

Beta blockers , enhance and mask the effects of hypoglycaemia

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5
Q

When is hydrocortisone used ?

A

For gluticocorticoid insufficiency in Addisons

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6
Q

What drug causes a transcriptional up regulation of gluconeogenesis and suppresses inflammatory response ?

A

Hydrocortisone

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7
Q

What are the common and long term ADRs of hydrocortisone ?

A

Weight gain, fluid retention, hypoglycaemia.

Long term causes Cushings

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8
Q

When can an Addisons px not be given hydrocortisone ? (3)

A

If immunosuppressed, diabetic or have an active fungal infection

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9
Q

What drug tx is commonly used for hypothyroidism?

A

Levothyroxine (T4). Synthetic thyroxine that is converted to T3.

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10
Q

When is Carbimazole used ?

A

For hyperthyroidism in Graves.

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11
Q

What is the MOA of Carbimazole ?

A

prodrug converted to methimazole. Inhibits thyroid peroxidase (blocks iodination of thyroglobulin needed for T3/T4).

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12
Q

A px is on a type of blood thinners. Which type should is contraindicated for Carbimazole (hyperthyroid tx) ?

A

Warfarin (Coumarin class drugs). Carbimazole may enhance anti coagulation effect.

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13
Q

What are catabolic reactions ?

A

Destroys reactants reducing big substances to smaller molecules. Energy releasing.

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14
Q

What are the general actions of Vits; B, C, K ?

A

B, important in ATP production from glucose
C, helps improve iron absorption
K, crucial to blood clotting

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15
Q

Which lipids are essential and why ?

A

Omega 3 and 6, can’t synthesise them so have to be ingested

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16
Q

What major group forms the bulk of CT ?

A

Proteins.

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17
Q

How many ATPs are produced in one cycle of cellular respiration ?

A

38

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18
Q

Which part of respiration is anaerobic , what happens to the pyruvate ?

A

Glycolysis, pyruvate then goes through fermentation.

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19
Q

What occurs in the islet of Langerhans during fasting ?

A

There’s low glucose so Glucagon is secreted from alpha cells. Catabolic shift releases glucose
Gluconeogenesis and glycogenolysis both ^.

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20
Q

What is the pathology in T1DM ?

A

Body isn’t making enough insulin, autoimmune response destroys b islet cells.

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21
Q

What happens to glucose when insulin levels are low?

A

Glucose can’t get into cells. Body tries to make more glucose to compensate but this worsens the problem. Glucose is then released through the kidneys.

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22
Q

What are the 4 T’s of T1DM sx ?

A

Thinner, thirst, toilet, tiredness

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23
Q

What is the pathology in T2DM ?

A

Fat deposits block effects of insulin on cell receptors. Pancreas ^ insulin -> BG ^ even though cells desperate for energy. Insulin wears out from overstimulation.

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24
Q

What are the common sx of T2DM and how do they arise ?

A

Blurred vision, thrush, genital itching

Slow onset, can go untreated for around 10 years.

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25
Q

What are the stages of diabetic retinopathy ?

A

No detonation, background retinopathy, proliferative retinopathy, maculotherapy.

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26
Q

Px presents with background diabetic retinopathy. They ask about their pathology and how you’re going to treat them ?

A

Pathology; BVs weaken , leak , bleed.

Tx; control BP and BG for prevention of further problems

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27
Q

Which stage of diabetic retinopathy shows circulation problems in BVs that leads to new BVs being formed?

A

Proliferative phase, new BVs to ^ O2 but they’re delicate so leak even more. ^ blood in retina -> floaters/loss of vision.

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28
Q

What is the problem during maculotherapy ?

A

Fluid in macula leaks through BVs. Contains fat and cholesterol that forms exudates when the H2O is reabsorbed.

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29
Q

What is the proper term for ‘yellow blobs’ seen too close to the centre of the eye and what problems arise ?

A

Exudates seen in maculotherapy. If fluid is too close to the centre the vision will be distorted

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30
Q

Why does peripheral neuropathy occur ?

A

Not enough glucose (insulin poor) leads to nerve signalling/cell damage. Pain signal transmission to the brain stops so unaware of pain in feet.

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31
Q

What is the name of the microvascular disease that leads to renal failure during diabetes ?

A

Diabetic nephropathy

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32
Q

How does diabetic nephropathy occur ?

A

Hyperfiltration and perfusion leads to hypoalbuminuria. This ^ afferent arteriole dilation (vasoconstriction down-lack of auto reg response). ^ interglomerular pressure -> ^ ECM production+mesengial cell hypertrophy. GFR/SA down for filtration –> renal failure.

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33
Q

What is the cause of glomerular sclerosis ?

A

Glomerula basement membrane thickens as a result of diabetic nephropathy

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34
Q

What are the main filtration layers of glomerulus ?

A

Vascular endothelium, covers inside of BV (endo wall)
Glomerular BM, surrounds VE
Visceral endo (podocytes)
Mesangium, in between capillaries. Produces collagen for support

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35
Q

How does an ^ in P in glomerulus lead to kidney failure?

A

mesangial expand and get damaged, cytokines release, O2 free radicals (endo dysfunction) leads to hypertrophy -> fenestrations expand so SA down. filtration becomes leaky proteins filtered out of blood -> Ischemia -> cell death

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36
Q

What are fenestrations ?

A

Spaces between podocytes. If small SA ^.

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37
Q

What are the two types of RAPD?

A

Relative afferent pupil defect
Direct response if light shined into eye
Consential if opposite eye

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38
Q

What are 3 common differentials when diagnosing RAPD?

A

MS (myelin degrades) , optic neuritis , severe cataracts

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39
Q

What simple test can be down to test for cataracts ?

A

Red reflex, also shows retinal blastoma.

If appears white then cataract present/further testing needed

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40
Q

What qualities are you looking for in the optic disc ? (3)

A

Colour , contour and cupping

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41
Q

How can you distinguish between the veins are arteries of the eye ?

A

Vein carriers more CO2 and less O2 so appears darker than arteries

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42
Q

What are the layers of the fovea ? (3)

A

Superficial to deep;

Ganglion cells, rods + cones , pigment layer

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43
Q

How might you know if a px has had laser therapy before ?

A

Blocks dots (scarring) may be present at the back of the retina wall.

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44
Q

What is the vitreous ?

A

Small jelly like structure found just inside the choroid

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45
Q

Which area of the eye has the most precise vision ?

A

Macula

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46
Q

How does the internal carotid artery branch to give blood supply to the eye ?

A

Branches to opthalmic artery which then gives off the central retinal , long posterior ciliary and short posterior ciliary

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47
Q

Through what structures does venous drainage of the eye occur ?

A

Vortex veins into the cavernous sinus

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48
Q

Which two muscles of the eye aren’t supplied by the oculomotor and which CN are they supplied by?

A

Superior oblique, CN 4

Lateral rectus, CN 6

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49
Q

What branch of the trigeminal nerve gives sensory info from eyelids, conjunctiva and cornea ?

A

V1 - ophthalmic

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50
Q

What is the ‘sense of spatial resolution’ ?

A

Ability of the eye to see 2 closely positioned objects as separate

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51
Q

What is the reading chart called and how are results recorded ?

A

Snellen chart. Read at 6m , recorded as distance/line read.

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52
Q

What do a swollen or cupped disc indicate respectively ?

A

Swollen = disc swelling

Cupping of the disc = glaucoma

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53
Q

How does retinal detachment occur and how would you see it under an ophthalmoscope ?

A

Retina appears whiter with distorted BVs

Tear in the retina -> fluid from vitreous goes through tear leading to elevation.

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54
Q

Apart from retinal detachment, what are the other major causes of DR ? (3)

A

Thickening of capillary BM, defective fibrinolysis, abnormal proliferation of capillary endothelium

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55
Q

How does ischemia of the retinal BVs lead to retinal detachment ?

A

^ VEGF release , neovascularisation occurs , fibrovascular binding , retinal detachment.

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56
Q

What are the major risk factors for DR ? (7)

A

Duration of diabetes, poor glycemic control, pregnancy, hypertension, renal disease, obesity, smoking

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57
Q

What is rubeosis iridis and when does it occur ?

A

New BVs form on surface of the iris, ^VEGF found at front of the eye
End stage diabetic eye disease

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58
Q

What is the tx of DR and how does it work ?

A

argon laser. reduces the ischemic load by burning retinal tissue

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59
Q

How does the anti VEGF tx of DR work ?

A

Injection in eye every 4/6 weeks. V expensive (£500/injection).

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60
Q

What drugs are used in anti VEGF therapy ?

A

Bevacizumab , Aflibercept. Ranibizumab used if eye has central retinal thickness >400 um.

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61
Q

Name the 2 adrenal glands

A

Cortex and medulla

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62
Q

How would the feedback mechanism rebalance cortisol levels after an initial decrease ?

A

Hypothalamus detects change and ^ CRH secretions. APG then ^ ACTH which stimulates the remaining cortex to ^ cortisol secretions so plasma cortisol returns to normal.

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63
Q

What are the local affects of an enlarge pituitary both upward and sideways ?

A

Upward, headaches with possible visual disturbance (if extends up to optic nerve) eg. bitemporal hemianopia
Sideways, CN palsy. Common loss of spatial awareness

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64
Q

What effect would an ^ in TRH have on the pituitary ?

A

Thyrotropin releasing hormone

^ TSH and prolactin secretion

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65
Q

What is the main function of somatostatin ?

A

Inhibits GH and other hormone secretion

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66
Q

What does severe hypothyroidism cause in males and females respectively in relation to prolactin ?

A

^ prolactin , disrupts female periods

Causes male discharge and erectile dysfunction

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67
Q

How would you treat prolactin hypothyroidism ?

A

Give a dopamine agonist, dopamine inhibits prolactin release

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68
Q

What hormones are secreted by the APG and where do each one of them act roughly ?

A 
FSH , LH -> gonads 
ACTH -> adrenal cortex
TSH -> thyroid
Prolactin -> mammary glands 
Endorphins (MSH) 
GH -> liver and most of body
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69
Q

What type of cells secrete GH ?

A

Somatotropic cells in bones and muscles. Promotes linear growth, regulation of fat muscle and bone mass

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70
Q

What is secreted from pars intermedia cells ?

A

MSH secreted (part of melanocytes)

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71
Q

How does GH deficiency effect children and adults respectively ?

A

Children , short stature or gigantism

Adults, decreased muscle mass, well being and performance or acromegaly

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72
Q

What effects do ADH and Prolactin deficiencies have ?

A

ADH -> diabetes insipidus (over urination and thirst)

Prolactin -> Sheehan’s syndrome, associated with failure of lactation

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73
Q

What is the action of TSH relating to Tg ?

A

TSH stimulates iodine uptake and iodination of tyrosine residues on Tg (thyroglobulin). Also binds to cell surface receptors to stimulate adenylate cyclase -> cAMP

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74
Q

How is TSH regulated ?

A

T4 exerts more -ve feedback >T3. When ^ levels of T4 produced from thyroid, acts on hypothalamus -ve.

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75
Q

Explain the thyroid blood test results in terms of hyper/hypo thyroidism and primary/secondary cause …

A 
Hyper = T3/T4 ^ , Hypo = T3/T4 low 
Primary = normal TSH (cause is gland) 
Secondary = abnormal (high/low) TSH (cause is pituitary)
76
Q

T3/T4; which is the predominant circulating hormone? which is deiondinated by the other? Which is more biologically active but with a shorter half life?

A

T4 dominant
T3 deiodinates T4
T3 is more biologically active but shorter half life

77
Q

What are the common aetiologies of hypothyroidism ? (4)

A

Primary thyroid failure (autoimmune eg. Hashimoto Thyroiditis) , idiopathic, ablative therapy, I deficiency

78
Q

When is the best time to measure ACTH levels for the being too high or too low ? How would you measure?

A

Too high = 12pm (should be lowest)
Too low = 9am (should be highest)
Measure through salivary cortisol (spit in tube)

79
Q

What is myxoedema coma and what tests can prove it ?

A

End stage hypothyroidism -> coma

TSH normal, T3/T4 down. ^ bilirubin, ALT, LDH, CK

80
Q

What is Graves disease ?

A

Hyperthyroidism, autoimmune thyroid stimulating antibodies. Shows heat intolerance, ^ bowel movements, fatigue, appetite down, anxiety ^ , irregular periods

81
Q

What is T3 toxicosis ?

A

Serum T3 ^ when both TSH and T4 are normal/low

82
Q

How would you treat hyperthyroidism and Graves ?

A

mild b blockers (e.g. propanolol)

Graves; antithyroid meds, radioactive iodine, thyroidectomy

83
Q

How does stress effect cortisol levels ?

A

stress/circadian rhythm act ^ freq on hypothalamus. ^ CRH/ADH -> ^APG -> ACTH^ -> Cortisol from adrenals

84
Q

What happens when cortisol is too ^ ?

A

Acts on APG/hypothalamus to oppose GH secretion +circadian rhythms

85
Q

What are the 3 areas of adrenal cortex from out to in and what do they secrete ?

A

Zona;
Glomerulus ; aldosterone
Fasicularis ; cortisol
Reticularis ; androgens (DHEA which is precursor)

86
Q

What is the action of aldosterone ?

A

^ regulates Na/K pumps. Reabsorption of Na/Cl/H2O into blood and secretion of K into urine.

87
Q

What are the clinical features of Addison’s ?

A

Progressive weakness, ^ pigmentation (^ACTH), hyperkalemia/hyponatremia , hypertension + dehydration.

88
Q

Measuring ACTH levels in Addison’s can indicate a key feature of the disease. What is it and what are the levels ?

A

^ ACTH shows 1st adrenal insufficiency

Low ACTH shows 2nd adrenal insufficiency

89
Q

What are the types of Addison’s disease ? (3)

A 
primary autoimmune adrenalitis , irregularly shrunken glands 
secondary hyperadrenalism (pituitary) adrenals small and flat
Metastic Cancer , leads to adrenals enlarged with architecture obscured.
90
Q

What is Cushing’s syndrome ?

A

endocrine disorder from ^ cortisol in the blood

91
Q

What are the 5 causes of Cushing’s syndrome ?

A 
Pituitary tumours that produce ACTH 
Ectopic ACTH benign/malignant tumour (outside normal pathway) 
Adrenal gland carcinoma benign
Adrenal gland carcinoma malignant 
Glucocorticoid drugs
92
Q

What cells secrete NA/A into the blood during extreme stress ? How are they stimulated ?

A

Chromaffin cells of the adrenal medulla, stimulated by preganglionc sympathetic neurones from spinal cord. A goes straight to target tissue.

93
Q

What are the major functions of NA/A ? (3)

A

Dumps glucose into blood prepares body for action, ^CV and metabolic function. Decreases GI and genitourinary function.

94
Q

How would you treat acromegaly and why ?

A

IGF-1 inhibited by somatostatin, give somatostatin analogues to ^ feedback of IGF-1.

95
Q

How would you diagnose acromegaly ?

A

OGTT (oral glucose tolerance test). Glucose suppresses IGF-1. Then do an MRI of pituitary to confirm.

96
Q

How would you tx precocious puberty ?

A

Long acting GnRH analogues (Leuprorelin) manipulate reproductive cycles.

97
Q

What are the action of V1 and V2 receptors ?

A

V1, regulate contraction of vascular SM through IP3/Ca

V2, regulate ADH through action of cAMP.

98
Q

What effect does age have on ADH levels ?

A

Age ^ ADH secretion, leading to H2O retention and hyponatremia

99
Q

What is the 5 step approach to ABG interpretation ? what are the normal ranges for the tested values

A

How is the px? eg. breathless
Assess oxygenation , PaO2 should be >10 kPa
Determine pH , normal range 7.35-7.45
Resp component, normal range 4.7-6.0 kPa
Metabolic component, normal range 22-26 mol

100
Q

How does the compensation time vary with respiratory and metabolic mechanisms ?

A

Respiratory is much faster

101
Q

if a px is given O2, what should their saturation levels be between ?

A

Should be about 10 kPa fewer than the percentage

102
Q

What can occur during ketoacidosis ?

A

Anion gap leads to xanthospasm and anaphylactic shock. This causes metabolic acidosis with respiratory failure.

103
Q

What are the ranges of HbA1c test for diabetic and pre diabetic ?

A

42-48 is pre

48+ is diabetic

104
Q

What do the muscles do as a response to vigorous exercise ?

A

Take up glucose after exercise to replenish glycogen stores.

105
Q

What substances exaggerate the glucose response after a meal ?

A

Incretins

106
Q

Why can’t you put a cannula directly into a vein ?

A

Septicaemia

107
Q

Why is C peptide thought to be a good measure of insulin ?

A

Not affected by hepatic insulin extraction.

108
Q

What is GLP-1, what is its function, where is it secreted from?

A

Its an incretin
Secreted upon ingestion of food from L cells of SI
^ glucose dependant insulin secretion, promotes satiety and decreases appetite and glucagon secretion.

109
Q

What is the effect of GLP-1 on the stomach ?

A

Delays gastric emptying. Nutrients delivered to SI and absorbed more smoothly. Decreases peak nutrient absorption, allows for insulin to be released gradually.

110
Q

What effects does GLP-1 have on the CNS ?

A

^ Satiety in CNS, this works to decrease food intake

111
Q

What enzyme can deactivate GLP-1 ?

A

DPP IV

112
Q

What is the best mode of entry for insulin in treatment?

A

SC, slow but safer for long term use. Should go to liver first but doesn’t
IM, difficult to self administer. Works faster and longer
IV, only lasts few minutes and ^ sepsis risk

113
Q

What is basal bolus insulin and when is it used ?

A

Insulin regime, young active lifestyle usually T1DM. Multiple injections with meals throughout the day.

114
Q

What is the name for pump therapy administration of insulin that is used in about 15% of px?

A

CSII (Continuous subcutaneous insulin infusion)

115
Q

Where does most of the H+ come from in the Henderson-Hasselbach equation ?

A

Most H+ is volatile acid produced from CO2. The carbonic acid is a weak acid buffer.

116
Q

What are the formulae for pH and pKa ?

A 
pH = - log10 (H+) 
pKa = -logKa
117
Q

How would you measure Carbonic acid levels in blood ?

A

Carbonic acid is transient in blood so difficult to measure (due to dissociation with carbonic anhydrase). So you measure pCO2 because the molar ratios are equal

118
Q

What is the normal pCO2 in arterial blood ?

A

5.1 kPa

119
Q

What is the ‘buffering line’ ?

A

The point at which equilibrium is reached at each pCO2, dependant on non HCO3 buffers (eg. Hb)

120
Q

What happens during respiratory alkalosis ?

A

eg. from a panic attack or hyperventilation. RR^ and CO2 down so curve moves right. loss of H+ so pH ^ as you loose HCO3- as buffer. Long term compensation retains HCO3 in kidneys.

121
Q

What is the compensatory mechanism during metabolic acidosis ?

A

DKA. RR ^ drains CO2 through Kussmaul ventilation (deep and laboured) leads to short term HCO3 down.

122
Q

What is the base excess ?

A

Quantity of base needed to be added to system in order to return to physiological normal.

123
Q

On a davenport diagram during metabolic problems what movement will be seen on the graph ?

A

Up or down the gradient of the curve (constant CO2)

124
Q

What would a left move of the curve on a davenport diagram represent ?

A

pCO2 change (in this case ^ CO2 has caused acidosis)

125
Q

What are the actions of phosphate and ammonia relative to buffering in the lumen ?

A

Phosphate is ‘filtered buffer’
Ammonia is ‘manufactured buffer’
^ HCO3 reabsorption and production. As buffer ^ in kidney you take up H+ in the lumen promoting the pump -> ^HCO3.

126
Q

What is the manufactured buffer ?

A

Ammonia, produced from glutamine (largely synthesised in PCT). NH3 secreted into lumen when acidic -> buffers H+ (forms NH4+) and stimulates pump so more HCO3/Cl absorbed

127
Q

What is the action of glutaminase enzyme ?

A

Converts glutamine into glutamate

128
Q

How would you tell the nature of a px’s respiratory acidosis ?

A

ventilation failure -> pCO2 ^ -> pH down. either initial buffer by carbonic acid/HCO3 and intracellular Hb or continuous extended through metabolic compensation (^NH3). Do they have any associated conditions eg. asthma = acute , COPD = chronic

129
Q

What is the renal response to metabolic acidosis (final line of defence) ?

A

Reabsorption of filtered HCO3. Max titration of filtered buffers and intrarenal synthesis of ammonia.

130
Q

How does hypokalaemia arise in metabolic acidosis ?

A

Upon presentation K is high but then it floods into blood and body cells become depleted despite overall high levels of K

131
Q

What is DKA and how can it commonly arise ?

A

High conc of ketone bodies from deamination of AA or ^ breakdown of fats. Alcoholism and dehydration from infection are common causes, obviously along with diabetes

132
Q

How can DKA arise from an anion gap ? (3)

A

Previously undiagnosed diabetes, interruption of insulin therapy (voluntary and non voluntary) , stress of recurrent illness

133
Q

What are the causes of dehydration ? (3)

A

Hyperglycaemia -> osmotic diuresis , hyperketonemia -> acidosis (vomiting) fluid/electrolyte imbalance, renal hyper perfusion (less able to deal with acidosis) H/ketone excretion down.

134
Q

What are the biochemical markers for DKA ? (5)

A

Hyperketonemia (>3mmol/l) ketonuria (++ or higher) leukocytosis (stress response indicator) hyperglycaemia (>11mmol/l) metabolic acidosis (pH <7.3 or HCO3 <15mmol/l)

135
Q

What happens to K during DKA?

A

K down but plasma conc may not reflect this. Low insulin means low permeability of cells to K, when insulin given K rushes out of cells. H2O down, K displaced from ICF

136
Q

Why shouldn’t you give saline for an extended period of time ?

A

Saline has pH of 5.5 so will cause acidosis

137
Q

How would you manage DKA in an emergency ?

A

Replace fluid loss with 0.9% saline, replace and monitor electrolytes to restore acid/base balance.
Insulin, infuse 0.1 u/Kg/Hr. monitor and regulate serum K (insulin may cause hypokalaemia)

138
Q

What is renal tubular acidosis ?

A

Failure of renal tube to secrete H due to proximal RTA defect in mechanism for HCO3 reabsorption of tube into blood.

139
Q

What is the significance of the ENAC transporter in RTA?

A

In certain forms of RTA it becomes damaged (inability to deal with the acid load)

140
Q

What are the common causes of respiratory alkalosis ? (4)

A

anxiety, drugs (that stimulate resp centre) , brain disorders, chronic liver disease

141
Q

What are the long term compensations of respiratory alkalosis ? (4)

A

HCO3 reabsorption inhibited, NH3 excretion down, net decrease in acid secretion and decrease plasma HCO3

142
Q

What is the tx for metabolic alkalosis ?

A

volume replacement (NaCl) as this switches off volume consuming measures (aldosterone).

143
Q

What are the two types of metabolic alkalosis ?

A

Hypovolaemic; gastric juices down, vomiting + gastric secretion (tx with diuretics)
Normovolaemic; HCO3 retention, Vol ^ in corticosteroid excess states (Cann’s, Cushing’s).

144
Q

What is the cause of normovolaemic Met Alky ?

A

decreased Na aggregates alkalosis and K decrease stimulating secretion so renal response is limited.

145
Q

What is Conn’s syndrome ?

A

Primary hyperaldosteronism , excess aldosterone -> low renin. Often caused by an adrenal gland tumour.

146
Q

What are the two conditions relating to a high or low level of Aldosterone ?

A

High - Conn’s

Low - Addison’s (also lack of cortisol)

147
Q

Why is the pH of urine significant ?

A

pH is around 6, body produces excess acid although total ‘acid load’ is regulated by the lungs (about 4x higher)

148
Q

What is the difference between weak and strong acids.?

A

Strong acids readily dissociate in water into H+ ions

149
Q

What is pK ?

A

The pH at which buffer works best to resist changes in either direction

150
Q

Which is better as a buffer and why; HCO3 or Hb ?

A

HCO3, it can deal with an almost infinite acid or base

151
Q

How are H and pCO2 measured ?

A

Using blood gas analyser (ion sensitive electrodes). Blood samples taken from brachial or radial artery using vacutainer (excludes air from sample).
Venous blood gas, not always accurate

152
Q

How does the pH change between in the lumen between the glomerulus and PCT?

A

Only slightly (7.4-7) due to carbonic anhydrase in lumen brush border. The epithelium is also leaky to H+.

153
Q

What is the name of the Na/H exchange carrier molecule and how is transport up regulated ?

A

NHE-3 (between lumen and glomerulus)

Up regulated by angiotensin 2 and when the pH falls.

154
Q

When does the absorptive state occur ?

A

0-4 hours post meal

155
Q

What can excess glucose be converted to in the absorptive state? (4)

A

Pentose phosphate -> NADPH+H+ , TAG synthesis in adipose and liver , FFA (fuel for muscle) , ^ protein synthesis due to ^ fuel for muscle.

156
Q

How is glucose converted in the pancreas ? what transporter does the pancreas use ?

A

Glucose -> Glucose-6-phosphate using glucokinase and 1 ATP (becomes ADP)
Uses the GLUT2 transporter (also in the liver)

157
Q

What is the significance of the GLUT2 transporter ?

A

^ Km than the other transporters so lower affinity for glucose. Only reaches max velocity when BG^ which alerts pancreatic beta cells to release insulin

158
Q

Apart from the liver and the pancreas, what enzyme is used as a detecter for blood glucose levels ?

A

Hexokinase

159
Q

What is significant about glucokinase enzyme ?

A

Not inhibited by G-6-P (its product) acts as signalling molecule to pancreas to produce insulin in ^ concentrations

160
Q

How can the body lower blood glucose without insulin ?

A

Liver doesn’t require stimulation from insulin, can take up BG and store it (primary store) or convert it into other products

161
Q

What is the action of insulin on the liver ?

A

Glucokinase dephosphorylated in the liver so G-6P ^ , transpose glucose in cell and destabilises it.

162
Q

Where does G-6-P go once it’s been produced in the liver or pancreas ?

A

Enters glycolysis or stored as glycogen.

163
Q

What is the key regulatory enzyme is glycolysis ?

A

PFK (phosphofructokinase). breaks down glucose if energy decreases (response to ATP).

164
Q

What substance overrides control of PFK, forcing glycolysis in the liver through action on phosphoprotein phosphatase ?

A

Insulin

165
Q

What is the effect of insulin on PFK and name the structure that it is attached to ?

A

Dephosphorylation
PFK and FBPase 2 are attached.
Insulin switches off FBPase and turns PFK on

166
Q

What happens when FBPase/PFK is dephosphorylated ?

A

Triggers F-2,6-BP formation which acts on glycolysis overriding PFK regulation so it ^.

167
Q

Apart from ^ glycolysis, what other actions does F-2,6-BP have ?

A

turns of gluconeogenesis. Tell liver to stop making glucose and ^ breakdown so BG drops

168
Q

What is the function of Acetyl CoA decarboxylase ?

A

Once dephosphorylated by insulin, it ^ FA’s production from acetyl CoA using excess glucose.

169
Q

How are tags (produced by the liver) packaged and exported ?

A

As VLDL , leads to atherosclerosis and CV disease

170
Q

What is the action of HDL ?

A

Takes excess cholesterol from tissue to the liver

171
Q

Where is lipoprotein lipase found and what is its action?

A

Found in lining of BVs. Recognises lipoproteins, cuts them away fat from within them (to be absorbed in tissues - adipose/muscle)

172
Q

At what points does a muscle use FAs and glucose ?

A

Uses glucose until 70% VO2 max then glucose when fats can’t be metabolised fast enough (O2 debt -> anaerobic resp)

173
Q

What receptors are present in adipose tissue ?

A

GLUT 1+3 (basal) and GLUT4 , this shows ^ response to insulin during exercise.

174
Q

What is brown adipocyte ?

A

Neonates use it to keep warm. Adults who retain it are more protected from obesity and diabetes.

175
Q

What is the function of the kidney during the post absorptive / starvation state ?

A

Used for making glucose through gluconeogenesis. Early fasting uses just liver then gradually uses more kidneys (renal medulla).

176
Q

What tests need to be done to confirm a px as diabetic ?

A

Fasting plasma glucose (>7mmol/L)
Random plasma glucose (>11.1mmol/L)
2 hr glucose post 75G GTT (glucose tolerance test , >11.1)

177
Q

Give an example when HbA1c would not be used for diabetic diagnosis ?

A

When the RBCs are abnormal eg. in sickle cell anaemia

178
Q

List some acute complications of diabetes … (3)

A

DKA, Hyperglycaemia, Hyperosmolar syndrome (HHS) formally HONK (hyperosmolar nonketoic coma)

179
Q

When is a px classified as ‘ketoanaemia’ ?

A

> 3 mmol/l or with urine ++

180
Q

During tx how should levels of BS, ketones, HCO3 and fluid change during DKA ?

A

BS need to fall at 3mmol/h
Ketones fall at 0.3 mmol/h
HCO3 ^ 3 mmol/h
Fluid, insulin, K all need to ^

181
Q

What insulin tx can cause hypoglycaemia ?

A

Sulphonylureas eg. gliclazide, glibenclamide

182
Q

How would you treat an adult in hypoglycaemia who is conscious, orientated and able to swallow ?

A

15-20g of quick acting carbs eg. 90ml of lucazade. Repeat up to 3x until BS >4. Once >4 give CHO and observe for 12-24 hrs.

183
Q

What problem would a px be experiencing if a doc issued them 20% glucose /100ml every 15 minutes, glucagon 1mg IM and then checked BG every 10 mins?

A

Unconscious hypoglycaemia, with/without seizures and aggression
follow up with long CHO or 10% glucose if still T-LOC

184
Q

Name some macrovascular complications of DM … (3)

A

Ischemic HD , peripheral vascular disease, stroke

185
Q

What is the difference between serum and plasma?

A

Fluid part of blood that doesn’t have coagulation factors

Plasma contains coagulated fx.

test (14 decks)

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