Case 10 Flashcards
(185 cards)
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
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.
3
Q
How would you treat an OD on insulin ?
A
Px is hypoglycaemic so tx with glucose and glucagon
4
Q
What group of drugs are contraindicated on insulin and why ?
A
Beta blockers , enhance and mask the effects of hypoglycaemia
5
Q
When is hydrocortisone used ?
A
For gluticocorticoid insufficiency in Addisons
6
Q
What drug causes a transcriptional up regulation of gluconeogenesis and suppresses inflammatory response ?
A
Hydrocortisone
7
Q
What are the common and long term ADRs of hydrocortisone ?
A
Weight gain, fluid retention, hypoglycaemia.
Long term causes Cushings
8
Q
When can an Addisons px not be given hydrocortisone ? (3)
A
If immunosuppressed, diabetic or have an active fungal infection
9
Q
What drug tx is commonly used for hypothyroidism?
A
Levothyroxine (T4). Synthetic thyroxine that is converted to T3.
10
Q
When is Carbimazole used ?
A
For hyperthyroidism in Graves.
11
Q
What is the MOA of Carbimazole ?
A
prodrug converted to methimazole. Inhibits thyroid peroxidase (blocks iodination of thyroglobulin needed for T3/T4).
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.
13
Q
What are catabolic reactions ?
A
Destroys reactants reducing big substances to smaller molecules. Energy releasing.
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
15
Q
Which lipids are essential and why ?
A
Omega 3 and 6, can’t synthesise them so have to be ingested
16
Q
What major group forms the bulk of CT ?
A
Proteins.
17
Q
How many ATPs are produced in one cycle of cellular respiration ?
A
38
18
Q
Which part of respiration is anaerobic , what happens to the pyruvate ?
A
Glycolysis, pyruvate then goes through fermentation.
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 ^.
20
Q
What is the pathology in T1DM ?
A
Body isn’t making enough insulin, autoimmune response destroys b islet cells.
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.
22
Q
What are the 4 T’s of T1DM sx ?
A
Thinner, thirst, toilet, tiredness
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.
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.
25
What are the stages of diabetic retinopathy ?
No detonation, background retinopathy, proliferative retinopathy, maculotherapy.
26
Px presents with background diabetic retinopathy. They ask about their pathology and how you're going to treat them ?
Pathology; BVs weaken , leak , bleed.
| Tx; control BP and BG for prevention of further problems
27
Which stage of diabetic retinopathy shows circulation problems in BVs that leads to new BVs being formed?
Proliferative phase, new BVs to ^ O2 but they're delicate so leak even more. ^ blood in retina -> floaters/loss of vision.
28
What is the problem during maculotherapy ?
Fluid in macula leaks through BVs. Contains fat and cholesterol that forms exudates when the H2O is reabsorbed.
29
What is the proper term for 'yellow blobs' seen too close to the centre of the eye and what problems arise ?
Exudates seen in maculotherapy. If fluid is too close to the centre the vision will be distorted
30
Why does peripheral neuropathy occur ?
Not enough glucose (insulin poor) leads to nerve signalling/cell damage. Pain signal transmission to the brain stops so unaware of pain in feet.
31
What is the name of the microvascular disease that leads to renal failure during diabetes ?
Diabetic nephropathy
32
How does diabetic nephropathy occur ?
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.
33
What is the cause of glomerular sclerosis ?
Glomerula basement membrane thickens as a result of diabetic nephropathy
34
What are the main filtration layers of glomerulus ?
Vascular endothelium, covers inside of BV (endo wall)
Glomerular BM, surrounds VE
Visceral endo (podocytes)
Mesangium, in between capillaries. Produces collagen for support
35
How does an ^ in P in glomerulus lead to kidney failure?
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
36
What are fenestrations ?
Spaces between podocytes. If small SA ^.
37
What are the two types of RAPD?
Relative afferent pupil defect
Direct response if light shined into eye
Consential if opposite eye
38
What are 3 common differentials when diagnosing RAPD?
MS (myelin degrades) , optic neuritis , severe cataracts
39
What simple test can be down to test for cataracts ?
Red reflex, also shows retinal blastoma.
| If appears white then cataract present/further testing needed
40
What qualities are you looking for in the optic disc ? (3)
Colour , contour and cupping
41
How can you distinguish between the veins are arteries of the eye ?
Vein carriers more CO2 and less O2 so appears darker than arteries
42
What are the layers of the fovea ? (3)
Superficial to deep;
| Ganglion cells, rods + cones , pigment layer
43
How might you know if a px has had laser therapy before ?
Blocks dots (scarring) may be present at the back of the retina wall.
44
What is the vitreous ?
Small jelly like structure found just inside the choroid
45
Which area of the eye has the most precise vision ?
Macula
46
How does the internal carotid artery branch to give blood supply to the eye ?
Branches to opthalmic artery which then gives off the central retinal , long posterior ciliary and short posterior ciliary
47
Through what structures does venous drainage of the eye occur ?
Vortex veins into the cavernous sinus
48
Which two muscles of the eye aren't supplied by the oculomotor and which CN are they supplied by?
Superior oblique, CN 4
| Lateral rectus, CN 6
49
What branch of the trigeminal nerve gives sensory info from eyelids, conjunctiva and cornea ?
V1 - ophthalmic
50
What is the 'sense of spatial resolution' ?
Ability of the eye to see 2 closely positioned objects as separate
51
What is the reading chart called and how are results recorded ?
Snellen chart. Read at 6m , recorded as distance/line read.
52
What do a swollen or cupped disc indicate respectively ?
Swollen = disc swelling
| Cupping of the disc = glaucoma
53
How does retinal detachment occur and how would you see it under an ophthalmoscope ?
Retina appears whiter with distorted BVs
| Tear in the retina -> fluid from vitreous goes through tear leading to elevation.
54
Apart from retinal detachment, what are the other major causes of DR ? (3)
Thickening of capillary BM, defective fibrinolysis, abnormal proliferation of capillary endothelium
55
How does ischemia of the retinal BVs lead to retinal detachment ?
^ VEGF release , neovascularisation occurs , fibrovascular binding , retinal detachment.
56
What are the major risk factors for DR ? (7)
Duration of diabetes, poor glycemic control, pregnancy, hypertension, renal disease, obesity, smoking
57
What is rubeosis iridis and when does it occur ?
New BVs form on surface of the iris, ^VEGF found at front of the eye
End stage diabetic eye disease
58
What is the tx of DR and how does it work ?
argon laser. reduces the ischemic load by burning retinal tissue
59
How does the anti VEGF tx of DR work ?
Injection in eye every 4/6 weeks. V expensive (£500/injection).
60
What drugs are used in anti VEGF therapy ?
Bevacizumab , Aflibercept. Ranibizumab used if eye has central retinal thickness >400 um.
61
Name the 2 adrenal glands
Cortex and medulla
62
How would the feedback mechanism rebalance cortisol levels after an initial decrease ?
Hypothalamus detects change and ^ CRH secretions. APG then ^ ACTH which stimulates the remaining cortex to ^ cortisol secretions so plasma cortisol returns to normal.
63
What are the local affects of an enlarge pituitary both upward and sideways ?
Upward, headaches with possible visual disturbance (if extends up to optic nerve) eg. bitemporal hemianopia
Sideways, CN palsy. Common loss of spatial awareness
64
What effect would an ^ in TRH have on the pituitary ?
Thyrotropin releasing hormone
| ^ TSH and prolactin secretion
65
What is the main function of somatostatin ?
Inhibits GH and other hormone secretion
66
What does severe hypothyroidism cause in males and females respectively in relation to prolactin ?
^ prolactin , disrupts female periods
| Causes male discharge and erectile dysfunction
67
How would you treat prolactin hypothyroidism ?
Give a dopamine agonist, dopamine inhibits prolactin release
68
What hormones are secreted by the APG and where do each one of them act roughly ?
```
FSH , LH -> gonads
ACTH -> adrenal cortex
TSH -> thyroid
Prolactin -> mammary glands
Endorphins (MSH)
GH -> liver and most of body
```
69
What type of cells secrete GH ?
Somatotropic cells in bones and muscles. Promotes linear growth, regulation of fat muscle and bone mass
70
What is secreted from pars intermedia cells ?
MSH secreted (part of melanocytes)
71
How does GH deficiency effect children and adults respectively ?
Children , short stature or gigantism
| Adults, decreased muscle mass, well being and performance or acromegaly
72
What effects do ADH and Prolactin deficiencies have ?
ADH -> diabetes insipidus (over urination and thirst)
| Prolactin -> Sheehan's syndrome, associated with failure of lactation
73
What is the action of TSH relating to Tg ?
TSH stimulates iodine uptake and iodination of tyrosine residues on Tg (thyroglobulin). Also binds to cell surface receptors to stimulate adenylate cyclase -> cAMP
74
How is TSH regulated ?
T4 exerts more -ve feedback >T3. When ^ levels of T4 produced from thyroid, acts on hypothalamus -ve.
75
Explain the thyroid blood test results in terms of hyper/hypo thyroidism and primary/secondary cause ...
```
Hyper = T3/T4 ^ , Hypo = T3/T4 low
Primary = normal TSH (cause is gland)
Secondary = abnormal (high/low) TSH (cause is pituitary)
```
76
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?
T4 dominant
T3 deiodinates T4
T3 is more biologically active but shorter half life
77
What are the common aetiologies of hypothyroidism ? (4)
Primary thyroid failure (autoimmune eg. Hashimoto Thyroiditis) , idiopathic, ablative therapy, I deficiency
78
When is the best time to measure ACTH levels for the being too high or too low ? How would you measure?
Too high = 12pm (should be lowest)
Too low = 9am (should be highest)
Measure through salivary cortisol (spit in tube)
79
What is myxoedema coma and what tests can prove it ?
End stage hypothyroidism -> coma
| TSH normal, T3/T4 down. ^ bilirubin, ALT, LDH, CK
80
What is Graves disease ?
Hyperthyroidism, autoimmune thyroid stimulating antibodies. Shows heat intolerance, ^ bowel movements, fatigue, appetite down, anxiety ^ , irregular periods
81
What is T3 toxicosis ?
Serum T3 ^ when both TSH and T4 are normal/low
82
How would you treat hyperthyroidism and Graves ?
mild b blockers (e.g. propanolol)
| Graves; antithyroid meds, radioactive iodine, thyroidectomy
83
How does stress effect cortisol levels ?
stress/circadian rhythm act ^ freq on hypothalamus. ^ CRH/ADH -> ^APG -> ACTH^ -> Cortisol from adrenals
84
What happens when cortisol is too ^ ?
Acts on APG/hypothalamus to oppose GH secretion +circadian rhythms
85
What are the 3 areas of adrenal cortex from out to in and what do they secrete ?
Zona;
Glomerulus ; aldosterone
Fasicularis ; cortisol
Reticularis ; androgens (DHEA which is precursor)
86
What is the action of aldosterone ?
^ regulates Na/K pumps. Reabsorption of Na/Cl/H2O into blood and secretion of K into urine.
87
What are the clinical features of Addison's ?
Progressive weakness, ^ pigmentation (^ACTH), hyperkalemia/hyponatremia , hypertension + dehydration.
88
Measuring ACTH levels in Addison's can indicate a key feature of the disease. What is it and what are the levels ?
^ ACTH shows 1st adrenal insufficiency
| Low ACTH shows 2nd adrenal insufficiency
89
What are the types of Addison's disease ? (3)
```
primary autoimmune adrenalitis , irregularly shrunken glands
secondary hyperadrenalism (pituitary) adrenals small and flat
Metastic Cancer , leads to adrenals enlarged with architecture obscured.
```
90
What is Cushing's syndrome ?
endocrine disorder from ^ cortisol in the blood
91
What are the 5 causes of Cushing's syndrome ?
```
Pituitary tumours that produce ACTH
Ectopic ACTH benign/malignant tumour (outside normal pathway)
Adrenal gland carcinoma benign
Adrenal gland carcinoma malignant
Glucocorticoid drugs
```
92
What cells secrete NA/A into the blood during extreme stress ? How are they stimulated ?
Chromaffin cells of the adrenal medulla, stimulated by preganglionc sympathetic neurones from spinal cord. A goes straight to target tissue.
93
What are the major functions of NA/A ? (3)
Dumps glucose into blood prepares body for action, ^CV and metabolic function. Decreases GI and genitourinary function.
94
How would you treat acromegaly and why ?
IGF-1 inhibited by somatostatin, give somatostatin analogues to ^ feedback of IGF-1.
95
How would you diagnose acromegaly ?
OGTT (oral glucose tolerance test). Glucose suppresses IGF-1. Then do an MRI of pituitary to confirm.
96
How would you tx precocious puberty ?
Long acting GnRH analogues (Leuprorelin) manipulate reproductive cycles.
97
What are the action of V1 and V2 receptors ?
V1, regulate contraction of vascular SM through IP3/Ca
| V2, regulate ADH through action of cAMP.
98
What effect does age have on ADH levels ?
Age ^ ADH secretion, leading to H2O retention and hyponatremia
99
What is the 5 step approach to ABG interpretation ? what are the normal ranges for the tested values
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
How does the compensation time vary with respiratory and metabolic mechanisms ?
Respiratory is much faster
101
if a px is given O2, what should their saturation levels be between ?
Should be about 10 kPa fewer than the percentage
102
What can occur during ketoacidosis ?
Anion gap leads to xanthospasm and anaphylactic shock. This causes metabolic acidosis with respiratory failure.
103
What are the ranges of HbA1c test for diabetic and pre diabetic ?
42-48 is pre
| 48+ is diabetic
104
What do the muscles do as a response to vigorous exercise ?
Take up glucose after exercise to replenish glycogen stores.
105
What substances exaggerate the glucose response after a meal ?
Incretins
106
Why can't you put a cannula directly into a vein ?
Septicaemia
107
Why is C peptide thought to be a good measure of insulin ?
Not affected by hepatic insulin extraction.
108
What is GLP-1, what is its function, where is it secreted from?
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
What is the effect of GLP-1 on the stomach ?
Delays gastric emptying. Nutrients delivered to SI and absorbed more smoothly. Decreases peak nutrient absorption, allows for insulin to be released gradually.
110
What effects does GLP-1 have on the CNS ?
^ Satiety in CNS, this works to decrease food intake
111
What enzyme can deactivate GLP-1 ?
DPP IV
112
What is the best mode of entry for insulin in treatment?
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
What is basal bolus insulin and when is it used ?
Insulin regime, young active lifestyle usually T1DM. Multiple injections with meals throughout the day.
114
What is the name for pump therapy administration of insulin that is used in about 15% of px?
CSII (Continuous subcutaneous insulin infusion)
115
Where does most of the H+ come from in the Henderson-Hasselbach equation ?
Most H+ is volatile acid produced from CO2. The carbonic acid is a weak acid buffer.
116
What are the formulae for pH and pKa ?
```
pH = - log10 (H+)
pKa = -logKa
```
117
How would you measure Carbonic acid levels in blood ?
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
What is the normal pCO2 in arterial blood ?
5.1 kPa
119
What is the 'buffering line' ?
The point at which equilibrium is reached at each pCO2, dependant on non HCO3 buffers (eg. Hb)
120
What happens during respiratory alkalosis ?
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
What is the compensatory mechanism during metabolic acidosis ?
DKA. RR ^ drains CO2 through Kussmaul ventilation (deep and laboured) leads to short term HCO3 down.
122
What is the base excess ?
Quantity of base needed to be added to system in order to return to physiological normal.
123
On a davenport diagram during metabolic problems what movement will be seen on the graph ?
Up or down the gradient of the curve (constant CO2)
124
What would a left move of the curve on a davenport diagram represent ?
pCO2 change (in this case ^ CO2 has caused acidosis)
125
What are the actions of phosphate and ammonia relative to buffering in the lumen ?
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
What is the manufactured buffer ?
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
What is the action of glutaminase enzyme ?
Converts glutamine into glutamate
128
How would you tell the nature of a px's respiratory acidosis ?
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
What is the renal response to metabolic acidosis (final line of defence) ?
Reabsorption of filtered HCO3. Max titration of filtered buffers and intrarenal synthesis of ammonia.
130
How does hypokalaemia arise in metabolic acidosis ?
Upon presentation K is high but then it floods into blood and body cells become depleted despite overall high levels of K
131
What is DKA and how can it commonly arise ?
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
How can DKA arise from an anion gap ? (3)
Previously undiagnosed diabetes, interruption of insulin therapy (voluntary and non voluntary) , stress of recurrent illness
133
What are the causes of dehydration ? (3)
Hyperglycaemia -> osmotic diuresis , hyperketonemia -> acidosis (vomiting) fluid/electrolyte imbalance, renal hyper perfusion (less able to deal with acidosis) H/ketone excretion down.
134
What are the biochemical markers for DKA ? (5)
Hyperketonemia (>3mmol/l) ketonuria (++ or higher) leukocytosis (stress response indicator) hyperglycaemia (>11mmol/l) metabolic acidosis (pH <7.3 or HCO3 <15mmol/l)
135
What happens to K during DKA?
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
Why shouldn't you give saline for an extended period of time ?
Saline has pH of 5.5 so will cause acidosis
137
How would you manage DKA in an emergency ?
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
What is renal tubular acidosis ?
Failure of renal tube to secrete H due to proximal RTA defect in mechanism for HCO3 reabsorption of tube into blood.
139
What is the significance of the ENAC transporter in RTA?
In certain forms of RTA it becomes damaged (inability to deal with the acid load)
140
What are the common causes of respiratory alkalosis ? (4)
anxiety, drugs (that stimulate resp centre) , brain disorders, chronic liver disease
141
What are the long term compensations of respiratory alkalosis ? (4)
HCO3 reabsorption inhibited, NH3 excretion down, net decrease in acid secretion and decrease plasma HCO3
142
What is the tx for metabolic alkalosis ?
volume replacement (NaCl) as this switches off volume consuming measures (aldosterone).
143
What are the two types of metabolic alkalosis ?
Hypovolaemic; gastric juices down, vomiting + gastric secretion (tx with diuretics)
Normovolaemic; HCO3 retention, Vol ^ in corticosteroid excess states (Cann's, Cushing's).
144
What is the cause of normovolaemic Met Alky ?
decreased Na aggregates alkalosis and K decrease stimulating secretion so renal response is limited.
145
What is Conn's syndrome ?
Primary hyperaldosteronism , excess aldosterone -> low renin. Often caused by an adrenal gland tumour.
146
What are the two conditions relating to a high or low level of Aldosterone ?
High - Conn's
| Low - Addison's (also lack of cortisol)
147
Why is the pH of urine significant ?
pH is around 6, body produces excess acid although total 'acid load' is regulated by the lungs (about 4x higher)
148
What is the difference between weak and strong acids.?
Strong acids readily dissociate in water into H+ ions
149
What is pK ?
The pH at which buffer works best to resist changes in either direction
150
Which is better as a buffer and why; HCO3 or Hb ?
HCO3, it can deal with an almost infinite acid or base
151
How are H and pCO2 measured ?
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
How does the pH change between in the lumen between the glomerulus and PCT?
Only slightly (7.4-7) due to carbonic anhydrase in lumen brush border. The epithelium is also leaky to H+.
153
What is the name of the Na/H exchange carrier molecule and how is transport up regulated ?
NHE-3 (between lumen and glomerulus)
| Up regulated by angiotensin 2 and when the pH falls.
154
When does the absorptive state occur ?
0-4 hours post meal
155
What can excess glucose be converted to in the absorptive state? (4)
Pentose phosphate -> NADPH+H+ , TAG synthesis in adipose and liver , FFA (fuel for muscle) , ^ protein synthesis due to ^ fuel for muscle.
156
How is glucose converted in the pancreas ? what transporter does the pancreas use ?
Glucose -> Glucose-6-phosphate using glucokinase and 1 ATP (becomes ADP)
Uses the GLUT2 transporter (also in the liver)
157
What is the significance of the GLUT2 transporter ?
^ 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
Apart from the liver and the pancreas, what enzyme is used as a detecter for blood glucose levels ?
Hexokinase
159
What is significant about glucokinase enzyme ?
Not inhibited by G-6-P (its product) acts as signalling molecule to pancreas to produce insulin in ^ concentrations
160
How can the body lower blood glucose without insulin ?
Liver doesn't require stimulation from insulin, can take up BG and store it (primary store) or convert it into other products
161
What is the action of insulin on the liver ?
Glucokinase dephosphorylated in the liver so G-6P ^ , transpose glucose in cell and destabilises it.
162
Where does G-6-P go once it's been produced in the liver or pancreas ?
Enters glycolysis or stored as glycogen.
163
What is the key regulatory enzyme is glycolysis ?
PFK (phosphofructokinase). breaks down glucose if energy decreases (response to ATP).
164
What substance overrides control of PFK, forcing glycolysis in the liver through action on phosphoprotein phosphatase ?
Insulin
165
What is the effect of insulin on PFK and name the structure that it is attached to ?
Dephosphorylation
PFK and FBPase 2 are attached.
Insulin switches off FBPase and turns PFK on
166
What happens when FBPase/PFK is dephosphorylated ?
Triggers F-2,6-BP formation which acts on glycolysis overriding PFK regulation so it ^.
167
Apart from ^ glycolysis, what other actions does F-2,6-BP have ?
turns of gluconeogenesis. Tell liver to stop making glucose and ^ breakdown so BG drops
168
What is the function of Acetyl CoA decarboxylase ?
Once dephosphorylated by insulin, it ^ FA's production from acetyl CoA using excess glucose.
169
How are tags (produced by the liver) packaged and exported ?
As VLDL , leads to atherosclerosis and CV disease
170
What is the action of HDL ?
Takes excess cholesterol from tissue to the liver
171
Where is lipoprotein lipase found and what is its action?
Found in lining of BVs. Recognises lipoproteins, cuts them away fat from within them (to be absorbed in tissues - adipose/muscle)
172
At what points does a muscle use FAs and glucose ?
Uses glucose until 70% VO2 max then glucose when fats can't be metabolised fast enough (O2 debt -> anaerobic resp)
173
What receptors are present in adipose tissue ?
GLUT 1+3 (basal) and GLUT4 , this shows ^ response to insulin during exercise.
174
What is brown adipocyte ?
Neonates use it to keep warm. Adults who retain it are more protected from obesity and diabetes.
175
What is the function of the kidney during the post absorptive / starvation state ?
Used for making glucose through gluconeogenesis. Early fasting uses just liver then gradually uses more kidneys (renal medulla).
176
What tests need to be done to confirm a px as diabetic ?
Fasting plasma glucose (>7mmol/L)
Random plasma glucose (>11.1mmol/L)
2 hr glucose post 75G GTT (glucose tolerance test , >11.1)
177
Give an example when HbA1c would not be used for diabetic diagnosis ?
When the RBCs are abnormal eg. in sickle cell anaemia
178
List some acute complications of diabetes ... (3)
DKA, Hyperglycaemia, Hyperosmolar syndrome (HHS) formally HONK (hyperosmolar nonketoic coma)
179
When is a px classified as 'ketoanaemia' ?
>3 mmol/l or with urine ++
180
During tx how should levels of BS, ketones, HCO3 and fluid change during DKA ?
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
What insulin tx can cause hypoglycaemia ?
Sulphonylureas eg. gliclazide, glibenclamide
182
How would you treat an adult in hypoglycaemia who is conscious, orientated and able to swallow ?
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
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?
Unconscious hypoglycaemia, with/without seizures and aggression
follow up with long CHO or 10% glucose if still T-LOC
184
Name some macrovascular complications of DM ... (3)
Ischemic HD , peripheral vascular disease, stroke
185
What is the difference between serum and plasma?
Fluid part of blood that doesn't have coagulation factors
| Plasma contains coagulated fx.
