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Case 10 Flashcards

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1
Q

Effect of Thyrotropin releasing hormone (TRH)

A

Thyroid stimulating hormone release from anterior pituitary

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2
Q

Proportion of anterior pituitary which secretes TSH

A

3-5%

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3
Q

Effect of GHRH

A

GH release from anterior pituitary

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4
Q

Effect of GnRH

A

Gonadotrophin release from anterior pituitary (LH and FSH)

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5
Q

Effect of corticotropin releasing hormone

A

ACTH release from anterior pituitary

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6
Q

GH deficiency in children

A

Short stature

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7
Q

GH deficiency in adults

A

Reduced muscle mass and performance

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8
Q

LH deficiency in men

A

Hypogonadism, reduced sperm count

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9
Q

LH deficiency in women

A

Hypogonadism, amenorrhoea

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10
Q

FSH deficiency

A

Infertile

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11
Q

TSH deficiency

A

Hypothyroidism

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12
Q

ACTH deficiency

A

Loss of pigmentation

Hypoadrenalism

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13
Q

Prolactin deficiency

A

Rare

Sheehan’s Syndrome - failure of lactation

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14
Q

Effects of TSH

A

Synthesis of Thyroglobulin (Tg)
Iodide ion uptake from blood into thyroid cells
Iodination of tyrosine residues on Tg - producing T4 and T3

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15
Q

T4

A

Thyroxine

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16
Q

T3

A

3,5,3’-Triiodothyronine

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17
Q

Predominantly circulating thyroid hormone

A

T4

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18
Q

Biologically active thyroid hormone

A

T3

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19
Q

Target for ACTH

A

Adrenal Gland
Adipocytes
Melanocytes

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20
Q

Target for GH

A

All tissues

Particularly liver

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21
Q

Target for FSH and LH

A

Gonads

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22
Q

Target for TSH

A

Thyroid gland

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23
Q

Zona glomerulosa

A

Release of Aldosterone

Outermost layer of adrenal cortex

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24
Q

Zona fasciculata

A

Release of cortisol

Middle layer of adrenal cortex

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25
Zona reticularis
Release of DHEA | Innermost layer of adrenal cortex
26
Sella Turcica
Bone within which the hypothalamus sits | "Turkish cellar"
27
Symptoms of upward extending enlarged pituitary
Headache Loss of visual acuity Bitemporal hemianopia (Compression of optic chiasm)
28
Enlarged pituitary causes
Headache
29
Causes of Hypothyroidism
Autoimmune - Hashimoto Thyroiditis Ablative therapy (destruction of thyroid tissue) Iodine deficiency Idiopathic
30
Symptoms of Hypothyroidism
``` Fatigue Weight gain Cold intolerance Constipation Menstrual irregularity Joint pain and muscle cramps Infertility ```
31
Signs of Hypothyroidism
``` Hypothermia Periorbital puffiness Oedema Hypothermia Rough, dry skin Bradycardia Peripheral neuropathy (delayed relaxation of ankle jerk) Loss of outer 1/3 of eyebrow Hoarseness ```
32
Function of thyroid hormones
Increase BMR Long bone growth and Neural maturation Increase sensitivity of body to catecholamines
33
Myxoedema Coma
End stage hypothyroidism (if poorly controlled) Elderly, obese female becoming increasingly withdrawn /sleepy/confused. Slips into a coma
34
Lab results for primary hypothyroidism
Low T4 High TSH Hyponatraemia Raised LFTs (Bilirubin, lactate dehydrogenase, creatinine kinase, ALT)
35
Euthyroid Sick Syndrome
Low T3 Normal T4 Normal or low TSH
36
Cause of hyperthyroidism with low TSH
``` Graves Disease (Autoimmune, thyroid stimulating antibodies) Nodular Goitre (older people) Hyperemesis gravidarum Post partum thyroiditis Post viral thyroiditis Drugs (amiodarone) ```
37
Cause of hyperthyroidism with high TSH
Resistance to thyroid hormone Drugs (amiodarone, heparin) TSH secreting pituitary adenoma Neonatal period
38
Signs/Symptoms of Hyperthyroidism
``` Heat intolerance and sweating Bulging eyes irregular Periods Fatigue Weight loss (increased appetite) Increased bowel movements Palpitations Tremor Poor concentration ```
39
Treatment of mild hyperthyroidism
Propanolol
40
Why is Propanolol used in treatment of mild hyperthyroidism?
Blocks action of catecholamines (which is increased by XS cortisol) Non-specific, acts on all cells in the body
41
Treatment of Graves disease
Antithyroid medications (Radioactive Iodine - isolation, not good for families) Thyroidectomy
42
Treatment of nodular goiters/adenomas causing hyperthyroidism
Radioiodine therapy
43
Why does Addison's Disease cause hyperpigmentation?
High ACTH Gives rise to MSH Stimulates melanocytes
44
Why does Addison's Disease cause anorexia?
High ACTH Gives rise to MSH Inhibits appetite
45
Signs/Symptoms of Addison's disease
``` Hyperpigmentation Anorexia/Weight loss Hyperkalaemia Hyponatraemia Weakness and fatigue Sexual dysfunction Hypotension Dehydration ```
46
Causes of Addison's Disease
``` Granulomas in adrenals (sarcoidosis, TB, fungal infection) Shrunken adrenals (Autoimmune Adrenalitis, IDDM, Metastatic cancer Secondary to pituitary problem ``` Plus Amyloidosis and Haemochromatosis
47
Lab findings in Addison's Disease
``` Hyperkalaemia Hyponatraemia Low cortisol High ACTH = primary Low ACTH = secondary ```
48
Synacthen Test
Measure serum cortisol Administer Synacthen and wait 60 minutes Measure serum cortisol Normally, serum cortisol should double in 60 minutes
49
Treatment of Addison's Disease
Cortisol replacement - Hydrocortisone | Aldosterone replacement - Fludrocortisone
50
Causes of Cushing's Disease
Pituitary tumour (secreting ACTH) Drugs - exogenous corticoids Adrenal adenoma/carcinoma (secreting Cortisol)
51
What is Cushing's Syndrome?
Hypercortisolism
52
Symptoms of Cushing's Syndrome specific to men
Erectile dysfunction | Decreased libido and fertility
53
Signs/Symptoms of Cushing's Syndrome
``` Weight gain/Obesity Fatty deposits (moon face and hump back) Thin skin (bruises easily) Increased thirst and urination Fatigue ```
54
Complications of Cushing's Syndrome
``` Increased risk of infection T2DM Bone loss/fracture Kidney stones Enlargement of pituitary tumour Hypertension (A and NA cause vasoconstriction) ```
55
What is pheochromocytoma?
Rare tumour of adrenal gland tissue
56
5Ps of Pheochromocytoma
``` Pressure (Hypertension) - 90% Pain - 80% Perspiration - 71% Palpitation - 64% Pallor - 42% ```
57
Classic Triad of Pheochromocytoma
Palpitations Perspiration Pain
58
Absorptive state occurs
0-4 hours after a meal
59
Processes which occur during absorptive state:
TAG synthesis Glycogenesis Glycerol synthesis Protein synthesis
60
How does pancreatic glucokinase differ from other hexokinases?
Not inhibited by its product - Glc-6-P
61
GLUT2
Glc transporter found in liver and pancreas Low affinity Works at high [Glc]
62
Glucokinase
Glc --> Glc-6-P
63
Where is UDP-glucose phosphorylase located?
Liver
64
UDP-Glucose Phosphorylase
Glc-6-P --> UDP Glc
65
PP-1 is activated by:
Insulin
66
Effect of PP-1
Upregulates glycogen production | Downregulates glycogenolysis
67
GLUT4
High affinity glucose transporter Found in adipose tissue and muscle Works at low [Glc]
68
Lipoprotein lipase
Cuts fatty acids from TAGs and transports them across capillary wall into cells
69
Lipoprotein Lipase is found in which cells
Luminal surface of capillary cells
70
Function of brown fat
Thermoregulation, | Protection against metabolic disease
71
Effect of exercise on GLUT4
Increase in number
72
GLUT4 is activated by:
Insulin
73
Function of carnitine shuttle
Allows Acetyl CoA to cross mitochondrial membrane so that it can enter the TCA cycle
74
Anabolism
Construction - consumes energy
75
Catabolism
Destruction - releases energy
76
Amino acids and glucose delivered to liver via
Hepatic Portal Vein
77
How do dietary TAGs reach the bloodstream?
Packaged into chylomicrons Enter lacteals Pass through thoracic duct into bloodstream
78
Action of insulin during Absorptive State
Uptake of amino acids and glucose into tissues Uptake of TAGs into adipose tissues Conversion of glucose to glycogen (activates glycogen synthase)
79
Action of glucocorticoids in post-absorptive state
Breakdown of protein and TAGs into glucose
80
Action of epinephrine in post-absorptive state
Breakdown of protein, glycogen and TAGs into glucose
81
Action of glucagon in post-absorptive state
Breakdown of glycogen into glucose
82
When does the body enter post-absorptive state?
After absorptive state | When enterocytes stop supplying portal hepatic circulation with glucose.
83
pK of a buffer
pH at which the buffer works best to resist changes in either direction.
84
Buffers found in renal tubules
Phosphate | Ammonia
85
3 Mechanisms of Renal Compensation
Bicarbonate reabsorption Net Acid Secretion Buffers (Phosphate and Ammonia)
86
Causes of respiratory acidosis
Asthma, COPD
87
Renal response to long term acidosis
Reabsorption of bicarbonate Secretion of H+ Synthesis of ammonia
88
Cause of Metabolic Acidosis
Diabetic Ketoacidosis
89
Immediate compensation for acidosis
Buffering in bloodstream
90
Time for respiratory response to occur in acidosis/alkalosis
Hours
91
Time for renal response to occur in acidosis/alkalosis
Days
92
Kussmaul respiration
Deep breathing pattern which drives CO2 below normal levels
93
Respiratory response to metabolic acidosis
Low pH detected by chemoreceptors in brainstem | Initiates deep breathing pattern (Kussmaul) to drive CO2 below normal level
94
Chemoreceptors which detect pH change in the blood are located...
Ventrolateral surface of the medulla
95
Factors which increase H+ secretion by kidneys
``` Increased HCO3- filtration by glomerulus Decreased extracellular volume (dehydration) Low blood pH High blood CO2 Low K+ Aldosterone ```
96
Cells in the renal tubules responsible for H+ secretion and HCO3- reabsorption
Alpha intercalated cells
97
Cells in renal tubules responsible for Na+ reabsorption and K+ secretion
Principal Cells
98
Effects of aldosterone
Increased K+ and H+ in urine | Increased HCO3- and Na+ in blood
99
Transporters activated by aldosterone
Na+/H+ ATPase exchange (in apical surface - lining lumen of tubule) Na+/K+ ATPase exchange (on capillary membrane)
100
Normal anion gap
HCO3- loss
101
Anion Gap
(Na+) - ((Cl-)+(HCO3-)) | Used to determine presence of unmeasured ions
102
Increased anion gap
Accumulation of organic acid (H+ and A-) or impaired H+ secretion
103
Mechanisms for normal anion gap
Inorganic addition - ingestion/infusion of inorganic acid (e.g. HCl) GI Base loss - severe diarrhoea, small bowel fistula, surgical diversion of urine into bowel Renal base loss AND acid secretion
104
Mechanisms for increased anion gap
``` Increased ketones (DKA or starvation ketosis) Lactic acidosis Renal failure (increased organic acids due to lack of buffering) Exogenous acid load (salicylate, methanol, ethylene glycol poisoning) ```
105
Effect of surgical diversion of urine into gut (bladder cancer) on bowel mucosa
Mucosa secretes KHCO3 to buffer H+ from urine
106
Anions raised in DKA
Acetoacetate and beta-OH butyrate
107
Anions raised in starvation ketosis
Acetoacetate and beta-OH butyrate
108
Anions raised in lactic acidosis
Lactate
109
Anions raised in renal failure
Organic acids
110
Methanol poisoning is commonly seen in...
Alcoholics
111
Ethylene glycol poisoning is commonly seen in..
Alcoholics
112
Anion raised in salicylate poisoning
Salicylate
113
Anion raised in methanol poisoning
Formate
114
Anions raised in Ethylene glycol poisoning
Glycolate and oxalate
115
Symptom of methanol poisoning
Visual disturbance
116
Sign of ethylene glycol poisoning
Oxallate Crystalluria
117
Ketones in ketoacidosis produced by...
Deamination of amino acids AND | Breakdown of fatty acids
118
Blood ketones in DKA
>3mmol/L
119
Blood glucose in DKA
>11mmol/L
120
Leukocytes in DKA?
Increased (stress response)
121
Ketones on urine dipstick in DKA
++
122
K+ depletion in DKA does not cause hypokalaemia because...
Patient is usually dehydrated
123
Treatment of DKA
0.9% saline (replace lost fluids) Insulin (0.1U/Kg/Hr) Replace and monitor electrolytes Restore acid:base balance
124
Considerations for Insulin treatment in DKA
SLOW infusion - since hypokalaemia may cause cerebral oedema Monitoring of K+ - since insulin increases cell permeability to K+, K+ enters cells causing hypokalaemia
125
Cause of PROXIMAL renal tubular acidosis
Defect in HCO3- reabsorption
126
Causes of DISTAL renal tubular acidosis
"Classical" - Defect in H+-ATPase pump "Hyperkalaemia" - Defect in Na+ transport across apical membrane, too little Na+ in cell for exchange for K+ in blood
127
Causes of respiratory alkalosis
``` Prolonged hyperventilation: Anxiety Drugs which stimulate respiratory centre (caffeine, nicotine) Brain disorders Chronic liver disease ```
128
Electrolyte imbalance caused by hypovolaemic metabolic alkalosis
Hypokalaemia (low K+)
129
Why does hypokalaemia cause H+ secretion?
Low K+ in blood Little Na+/K+ exchange occurs across capillary membrane Low K+ in intercalated cell High K+/H+ exchange across apical membrane (K+ in, H+ out) Increased H+ in tubular lumen for excretion
130
Why is respiratory response to metabolic alkalosis limited?
Hypoventilation cannot be sustained due to hypoxia
131
Renal response to hypovolaemic metabolic alkalosis
Na+ and HCO3- reabsorption in PCT Aldosterone release H+ secretion in DCT NH3 synthesis
132
Management of hypovolaemic metabolic alkalosis
Volume management - switch of volume conserving mechanisms which exacerbate alkalosis K+ replacement
133
Causes of normovolaemic metabolic alkalosis
``` Conn's syndrome (hyperaldosteronism) Cushing's syndrome (hypercortisolaemia - cortisol has similar effects to aldosterone) Renal hypoperfusion (low GFR = low HCO3- filtration) ``` i.e. Anything which causes HCO3- retentio
134
Symptoms of T1DM
Tiredness Polydipsia Polyuria Weight loss Candidal infection/Thrush (oral/genital due to high sugar environment)
135
Criteria for DM diagnosis
HbA1c >6.5% Fasting plasma glucose >7.0mmol/L Random plasma glucose >11.0mmol/L
136
GTT
Glucose tolerance test - Plasma glucose 2 hrs after administering 75g of glucose
137
Symptoms of T2DM
``` Polydipsia Polyuria Weight gain Blurred vision Candidal infection ```
138
Incidence
Occurrence of new cases
139
Prevalence
Proportion of cases in the population at a given time
140
Ethnic group affected by Type 1 diabetes
Caucasian especially scandinavian
141
Ethnic group affected by Type 2 diabetes
Non caucasians especially indigenous people, S. Indians and W. Indians
142
Incidence of T1DM
1/10,000
143
Incidence of T2DM
2/1000 per year
144
Anti-Islet Cell Antibodies associated with T1DM
Anti-GAD65 (85%) Anti-IA2 (55%) Anti-Insulin (50%) Anti-ZnT8 (50%)
145
Immune Cells responsible for destruction of Beta Cells in T1DM
T cells
146
Genes commonly associated with T1DM
HLA DR3/4 (Code for MHCs)
147
Environmental factors affecting T1DM
Breastfeeding Childhood infection Neonatal colonisation
148
Glucose level with increased risk of hyperosmolar coma
>30mmol/L
149
Hypoglycaemia
<4mmol/L (LOC occurs <2.5mmol/L)
150
Normal BG
4-8mmol/L
151
Hyperglycaemia
>8mmol/L
152
Blood pressure in DKA
Low (<90)
153
Oxygen saturation in DKA
Low (<92%)
154
Glasgow Coma Scale in DKA
Low (<12)
155
Causes of death in DKA
``` Cerebral oedema (due to hypokalaemia) Other underlying conditions - sepsis, MI, acute respiratory syndrome ```
156
Sulphonylureas
e.g. Gliclazide, Glibenclamide | Increased insulin release from beta cells in pancreas
157
Cause of hypoglycaemia in non-insulin-dependent diabetes?
Sulphonylureas | Metformin
158
Treatment of conscious (able to swallow) patient with hypoglycaemia
15-20g of quick acting CHO - repeat 3 times or until BG>4mmol/L e.g. Dextrose, lucozade, sugar When BG>4mmol/L, administer long acting CHO e.g. biscuits, bread, milk
159
Treatment of unconscious/aggressive patient with hypoglycaemia
``` Parenteral glucose (20%: 75-100ml in 15 mins OR 10%: 150-200ml in 15 mins) I/M Glucagon - 1mg ``` Check BG and repeat insulin infusion if BG<4mmol/L Do not repeat glucagon Follow up with long acting carbohydrate (or 10% glc if NBM)
160
Formation of exudates in diabetic retinopathy
Hyperglycaemia causes osmotic damage to retinal pericytes. Increased permeability of capillary walls Leakage of proteins and lipids into retinal tissue (+Foamy macrophages filled with lipid are deposited in under perfused capillary beds)
161
Formation of microaneurysms in diabetic retinopathy
Hyerglycaemia causes osmotic damage to retinal pericytes | Weakening of capillary walls allows focal dilatation i.e. microaneurysm.
162
Formation of cotton wool spots in diabetic retinopathy
Exudates and microaneurysms cause occlusion of vessels. | Ischaemic tissue appears white and fluffy i.e. cotton wool spot
163
Vitreous haemorrhage in diabetic retinopathy
Ischaemic cells produce VEGF which stimulates formation of new vessels. New vessels are thin walled and prone to bleeding.
164
Complication of vitreous haemorrhage
Site-threatening
165
Macular Oedema in diabetic retinopathy
Hyperglycaemia causes osmotic damage to retinal pericytes. Weaker, more permeable capillary walls. Leakage of fluid from capillary into retinal tissue
166
Visual impairment in Macular Oedema
Loss of central vision
167
Retinal Detachment in Diabetic Retinopathy
Collagen formation along the length of new, thin-walled vessels. Form fibrotic bands which will contract to detach the retina
168
Prevention of Vitreous Haemorrhage
Pan retinal photocoagulation | Anti-VEGF treatment
169
Mesangial expansion
Endothelial expansion and inflammation caused by free radicals and cytokines
170
Mechanism for Proteinuria in diabetic nephropathy
Trauma and damage to kidney nephrons due to increased GFR Release of cytokines and free radicals Causes mesangial expansion Larger fenestrations, larger molecules inc. proteins filtered out of blood into kidney tubules
171
Mechanism for Renal Failure in diabetic nephropathy
Hyperglycaemia activates RAAS Vasoconstriction of efferent arteriole Reduced perfusion of renal tubules - ischaemia Atrophy of vessels which support renal function
172
Mechanism for neuropathy in diabetes
Hyperglycaemia causes formation of sorbitol and fructose in Schwann cells Loss of structure and function of schwann cells Segmental demyelination
173
Diabetic Amyotrophy
Painful wasting of quadriceps | Reflexes may be reduced or absent
174
Acute, painful neuropathy
Burning or crawling pain in feet, shins or anterior thighs | May be worse at night
175
Symmetrical mainly sensory, polyneuropathy
Loss of vibration sense and proprioception Loss of temperature and pain sensation in extremities May have unrecognised trauma (ulcers on feet)
176
Multiple mononeuropathy
Isolated nerve palsies - often CNIII and CNVI
177
Autonomic effects of neuropathy
GI - gastroparesis, diarrhoea, incontinence Cardiovascular(vagus nerve affected) - postural hypotension, diminished vagal reflex, arrhythmia Bladder - incomplete emptying and stasis Male erectile dysfunction
178
Purpose of measuring HbA1c
Assesses long term control of blood glucose (average over 6 weeks) Useful in assessing risk of complications
179
Short-acting insulin
Lispro, Aspart, Glulisine
180
Long-acting insulin
NPH, Determir, Glargine
181
Function of sclera
Attachment for extraocular muscles which move the eye
182
Function of cornea
Refracts light entering the eye
183
Function of choroid
Vascular layer | Nourishes outer layers of retina
184
Structure of retina
Inner neural layer - containing photoreceptors | Outer pigmented layer - attached to choroid, continuing around whole inner surface of eye.
185
Macula
Centre of retina | High acuity vision - for reading and driving
186
Fovea
Depression in the centre of macula | Contains a high concentration of cones (light detecting cells) for sharp central vision
187
What is Glaucoma?
Obstruction of drainage of aqueous humor. | Drainage normally occurs via trabecular mesh network.
188
Blood supply of eye
Ophthalmic artery | Central artery of retina (supplies internal surface of retina - occlusion quickly causes blindness)
189
Sign of glaucoma
Increase in size of optic disc
190
Symptoms of retinal detachment
Blurred vision Dark areas Black or white flecks/strings in front of eyes
191
Risk factors for retinal detachment
Family history >40 years old Trauma
192
Features of background diabetic retinopathy
Dot and blot haemorrhages | Hard exudates
193
Features of preproliferative diabetic retinopathy
``` Venous beading Cotton wool spots Some new vessels More dot and blot haemorrhages Microaneurysms ```
194
Features of proliferative diabetic retinopathy
More new vessels
195
When do we refer diabetic retinopathy to secondary care?
Haemorrhages/Microaneurysms in 4 quadrants Venous beading in 2 or more quadrants IRMA (new vessels) in 1 or more quadrants
196
When do we treat diabetic retinopathy?
Thickening of retina or hard exudates within 500micrometers of centre of macula Zones of retinal thickening the size of the optic disc
197
Ranibizumab
Monoclonal antibody which inhibits VEGF. | Used in treatment of diabetic retinopathy.
198
Indication for hydrocortisone
Addison's Disease (chronically low cortisol)
199
ADRs for hydrocortisone
Weight gain Fluid retention Hyperglycaemia Cushing's (long term)
200
Contraindications for Hydrocortisone
Immunosuppression Diabetes Active fungal infections
201
Actions of Hydrocortisone
Upregulates gluconeogenesis - increases blood sugar | Suppresses inflammatory immune responses
202
Binding site of Levothyroxine
Nuclear thyronine receptors
203
What is levothyroxine?
Synthetic T4 which will be converted to T3 in the body
204
Indication for levothyroxine
Hypothyroidism
205
ADRs of levothyroxine
``` Tremor Cardiac arrhythmias Excitability Diarrhoea Flushing ```
206
Contraindications of Levothyroxine
Graves (Hyperthyroidism) Ischaemic Heart disease Thyrotoxicosis
207
Indication for carbimazole
Hyperthyroidism
208
MOA of Carbimazole
Thyroid peroxidase inhibitor | Enzyme which normally allows iodinisation of Tg, synthesising thyroid hormones
209
ADRs of Carbimazole
``` Fever Headache Rash Joint pain Taste disturbance ```
210
Contraindication of Carbimazole
Warfarinised - drug may enhance anticoagulation

Year 2 (17 decks)

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