Endocrinology Flashcards
(543 cards)
1
Q
What are features of Kallman syndrome?
A
- Delayed pubtery
- Hypogonadism
- Loss of smell
- Low sex hormones
- Normal/above average height
2
Q
How is Kallman syndrome managed?
A
- Testosterone supplementation
- Sex hormones supplementation for fertility
3
Q
What is vitamin D deficiency associated with?
A
Hypocalcaemia
4
Q
Patients with high calcium, low PTH with cancer risk factors?
A
Think malignancy
5
Q
What hormones does anterior pituitary produce?
A
ACTH, TSH, LH, FSH, PRL. GH, MSH
6
Q
What hormones does posterior pituitary produce?
A
ADH and oxytocin
7
Q
What is the management of hypoglycaemia with impaired GCS?
A
IV Glucose if access
8
Q
What characterises tertiary hyperparathyroidism?
A
- extremely high PTH
- moderately raised calcium
9
Q
What is the management of new onset graves disease to control symptoms?
A
- Propranolol
- Carbimazole used to induce remission
10
Q
Any change in vision for someone with thyroid eye disease needs what?
A
Urgent review by specialist
11
Q
What is the target HBa1c for those on hypoglycaemic medications for T2DM?
A
53
12
Q
What conditions make up MEN Type 2?
A
Medullary thyroid cancer, hypercalcaemia - parathyroid hyperplasia, phaeochromocytoma
13
Q
What is the mode of action of orlistat?
A
inhibiting gastric and pancreatic lipase to reduce the digestion of fat
14
Q
What should patients on long-term steroids do during intercurrent illness?
A
Double steroid doses
15
Q
What adjunct can be used alongside orlistat for obese patients with one weight related co-mobidity?
A
Liraglutide
16
Q
Subclinical hyperthyroidism is associated with what?
A
atrial fibrillation, osteoporosis and possibly dementia
17
Q
What should be monitored to detect recurrence of medullary thyroid cancer?
A
Serum calcitonin
18
Q
What is definitive management of primary hyperparathyroidism?
A
Total parathyroidectomy
19
Q
What is primary hyperparathyroidism?
A
XS secretions of PTH resulting in hypercalcaemia.
20
Q
When is primary hyperparathyroidism typically diagnosed?
A
Incidental finding of elevated serum Ca.
21
Q
Causes of primary hyperparathyroidism?
A
85% parathyroid adenoma. Others: hyperplasia, multiple adenoma, carcinoma.
22
Q
Primary hyperparathyroidism CP
A
- 80% asymptomatic
- ‘bones, stones, abdominal groans and psychic moans’
- polydipsia, polyuria, depression, anorexia, nausea, constip, peptic ulcer, pacreatitis, bone pain/fracture, renal stones, HTN
23
Q
Primary hyperparathyroidism associations
A
HTN, multiple endocrine neoplasia (MEN I and II)
24
Q
Primary hyperparathyroidism Ix
A
- Bloods
- Technetium-MIBI subtraction scan
- X-ray: pepperpot skull; osteoitis fibrosa cystica
25
Primary hyperparathyroidism bloods
Raised Ca, low phosphate,
PTH raised or normal (inappropriately given the raised calcium)
26
Primary hyperparathyroidism- when would conservative management be offered?
If the Ca is <0.25mmol/L above the limit of normal AND the pt is >50yrs AND there is no evidence of end organ damage
27
Primary hyperparathyroidism- what if the pt isn't suitable for surgery?
May be treated with cinacalcet (a calcimimetirc that mimics the action of calcium on tissues by allosteric activation of calcium-sensing receptor)
28
What is primary hypoparathyroidism?
Decrease PTH surgery eg. secondary to thyroid surgery
29
Primary hypoparathyroidism Mx
Alfacalcidol
30
Calcium and phosphate in primary hypoparathyroidism?
Low calcium, high phosphate
31
Main symptoms of hypoparathyroidism are secondary to what?
Hypocalcaemia (so CP is same as hypocalcaemia)
32
Pseudohypoparathyroidism?
Target cells being insensitive to PTH; due to abnormality in G protein; associated with low IQ, short stature, shortened 4th and 5th metacarpals.
33
Pseudohypoparathyroidism electrolyte levels?
Low calcium, high phosphate, high PTH
34
Pseudohypoparathyroidism diagnosis?
Infusion of PTH then measure urinary cAMP and phosphate levels. In hypoparathyroidism it'll increase. In psuedohypoparathyroidism type I they won't increase but in type II only cAMP rises.
35
Pseudopseudohypoparathyroidism?
Similar phenotype to pseudohypoparathyroidism but normal biochemistry
36
Confusion, hypothermia, hyporeflexia, bradycardia, seizures and signs of hypothyroidism?
Myoxedema coma
37
Patients with type I diabetes and a BMI > 25 should be considered for what?
Metformin alongside insulin
38
Asymptomatic patients with abnormal HbA1c/fasting glucose need what?
Second abnormal reading
39
hypothyroidism + goitre + anti-TPO triad suggests what?
Hashimotos thyroiditis
40
Thyrotoxicosis with tender goitre and raised ESR?
Subacute thyroiditis (De Quervains)
41
What are sick day rules for T1DM?
- Insulin should not be stopped
- Increased frequency of checking blood sugars
- Drink atleast 3L fluids
- Replace meals with carbohydrate drinks if appetite is reduced
42
What are sick day rules for T2DM?
- Stop oral hypoglycaemics and restart once eating and drinking is back to normal for 24-24 hours
- Do not stop insulin if using
- Monitor blood glucose more frequently as needed
43
Which drugs can cause galactorrhoea?
- Metoclopramide, domperidone
- Haloperidol
44
Who should diabetic foot problems be referred to?
Local diabetic foot centre
45
What does a patchy uptake on nuclear scintigraphy suggest?
Toxic multinodular goitre
46
Long term steroid use can lead to what?
Avascular necrosis
47
Steroids can cause what in the muscles?
Proximal myopathy
48
Which hormones are decreased in response to stress?
- Insulin
- Testosterone
- Oestrogen
49
What are the features of sick euthyroid syndrome?
Low T3/T4 with normal TSH during acute illness
50
What imaging should be done for those with suspected Cushings syndrome?
CT adrenal glands
51
Cushing' syndrome?
Prolonged high levels of glucocorticoids in body (CORTISOL).
52
Cushing's disease?
Cause of cushing's syndrome. When a pituitary adenoma secreting XS ACTH stimulates XS cortisol release from adrenal glands.
53
Causes of Cushing's syndrome?
- ACTH independent causes= Iatrogenic (corticosteroid therapy), adrenal adenoma (adrenal tumour secreting XS cortisol)
-ACTH dependent causes= pituitary adenoma secreting XS ACTH (CUSHING's DISEASE), paraneoplastic syndrome (eg. small cell lung ca secreting ACTH)
54
Cushing's syndrome CP?
Round puffy face (moon face), central obesity, abdo striae, proximal muscle wasting, hirsutism, hyperpigmentation of skin if Cushing's disease (high ACTH levels), depression, insomnia
55
Metabolic effects of Cushing's syndrome?
- hypokalaemic metabolic alkalosis
- impaired glucose tolerance
- HTN, DMT2, cardiac hypertrophy, osteoporosis, dyslipidaemia (raised cholesterol and triglycerides)
56
Body's normal response to dexamethasone?
Suppressed cortisol due to -ve feedback on hypothalamus. Reduces corticotropin releasing hormone (CRH) output. The lower CRH and ACTH levels result in low cortisol output by adrenal glands.
57
What is the response to dexamethasone in somebody with Cushing's syndrome?
Lack of cortisol suppression
58
Why does a high level of ACTH cause skin pigmentation?
Stimulates melanocytes in skin to produce melanin.
Pigmentation= Cushing's disease or ectopic ACTH.
No pigmentation= adrenal adenoma or exogenous steroids.
59
Cushing's syndrome Ix?
1) low-dose overnight dexamethasone supression test= if cortisol not supressed then...
- high-dose 48hr test= if cortisol suppressed (ACTH high) then Cushing's disease (pituitary adenoma), if not suppressed then adrenal adenoma (ACTH low) or ectopic ACTH (ACTH high).
2) Also do 24hr urinary free cortisol
3) CT adrenals if not suppressed and ACTH low
4) U&Es may show low K+ if adrenal adenoma also secreting aldosterone
60
Cushing's syndrome Mx?
- Transphenoidal resection of pituitary adenoma
- Surgical resection of adrenal adenoma/ectopic ACTH source
- If not possible= adrenalectomy + life long steroid replacement therapy
- occasionally Metyrapone used to reduce production of cortisol in adrenals
61
Nelson's syndrome?
Development of ACTH-prouding tumour following surgical removal of both adrenals glands due to lack of cortisol and -ve feedback. Causes skin pigmentation (high ACTH), bitemporal hemianopia and lack of other pituitary hormones.
62
Pseudo-Cushings?
Mimics cushings. Often due to alcohol XS or severe depression. Causes false +ve dexamethasone supression test or 24hr urinary free cortisol. Insulin stress test may be used to differentiate.
63
2nd line medication for obese patient with T2DM?
DPP-4 inhibitors as least likely to cause weight gain
64
What would be seen on thyroid scintigraphy for someone with De Quervains thyroiditis? (the Ix)
Reduced iodine uptake
65
Peptic ulceration, galactorrhoea, hypercalcaemia all suggest what?
MEN type 1(pancreas, parathyroid, pituitary)
66
Glucocorticoid therapy can induce what?
Neutrophilia
67
What would be the urine osmolality for someone with primary polydipsia?
-Initially low
- After fluid deprivation: High
68
What features would be atypical for suspected T1DM?
- Age > 50
- BMI > 25
- Slow progression of hyperglycaemia
69
What tests should patients undergo if atypical presentation of T1DM?
- C peptide and diabetic autoantibodies
70
What is the treatment of a thyrotoxic storm?
- Beta blockers, IV fluids, propylthiouracil and steroids
71
What should women with hypothyroidism do when they are pregnant?
Increase thyroid hormone replacement by upto 50%
72
Presentation of HHS
1) Hypovolaemia
2) Hyperglycaemia
3) Significantly raised serum osmolarity
4) Absence of ketoacidosis.
73
What blood sugars suggest impaired fasting glycaemia?
Between 6.1 and 6.9
74
What are the target blood sugars for T1DM?
Waking - 5-7
Other times: 4-7
75
What can worsen thyroid eye disease in patients with Graves?
Radioiodine treatment
76
What does a raised C-peptide help to distinguish?
Raised - T2DM
Low = T1DM
77
Management of subclinical hypothyroidism?
Check TPO antibodies
78
If 3 diabetic drugs are not helping, what should be done?
Switch one of them for a GLP-1 e.g. exenatide
79
Side effect of piogliotazone
Peripheral oedema
80
Patient who have 2 hypoglycaemic episodes need what?
Surrender driving licence
81
How should steroid doses be altered during illness with Addisons?
Glucocorticoid e.g. hydrocortisone -> doubled
Fludrocortisone -> kept the same
82
What are the diabetic specific autoantibodies?
anti-GAD
83
Which diabetes med increases risk of bladder cancer?
Thiazolidinedione e.g Pioglitazone
84
Over replacement with thyroxine increases the risk of what?
Osteoporosis
85
Fluids resuscitation in DKA?
1L of IV 0.9% NaCl over 1 hour - if systemic BP >90
500ml of IV 0.9% NaCl over 5 mins if systemic BP <90
86
What would be the expected metabolite results in Cushings?
Hypokalaemia with metabolic alkalosis
87
Erratic blood glucose control, bloating and vomiting
Gastroparesis
88
What should every person with insulin be given for emergencies?
Glucagon kit
89
Headaches, amenorrhoea, visual field defects suggests what?
Prolactinoma
90
Thyrotoxicosis with tender goitre?
De Quervains thyroiditis
91
Elevated prolactin with secondary hypothyroidism and hypogonadism?
Non-functioning pituitary adenoma
92
increased TSH levels and normal T4 suggests what?
Poor compliance with thyroxine
93
What can mimic Cushings disease?
Excess alcohol consumption
94
Increased plasma 17-hydroxyprogesterone levels is suggestive of what?
Congenital adrenal hyperplasia
95
Primary vs secondary hyperaldosteronism?
If renin is high, secondary cause is likely i.e. renal artery stenosis
96
hyponatraemia, reduced plasma osmolality and increased urine osmolality suggests what?
SIADH
97
Acromegaly?
XS GH secondary to a pituitary adenoma in over 95% of cases.
98
Symptoms of acromegaly?
- Spade like hands and feet
- Frontal bossing
- Macroglossia
- Headaches
- Bitemporal hemianopia
- Sleep disturbances
- Carpal tunnel
- HTN
- increased shoe size
- sweaty oily skin (sweat gland hypertrophy)
- 6% have MEN-1
99
What is the main cause of death in patients with acromegaly?
CVD
100
Cx of Acromegaly?
HTN, diabetes, cardiomyopathy, colorectal cancer
101
Ix for Acromegaly?
- 1st= serum IGF-1 levels; if raised then...
- Diagnostic test= Oral glucose tolerance test (shows no supression of GH)
- MRI may show pituitary tumour
102
Why are GH levels not diagnostic for acromegaly?
They vary throughout the day
102
How do somatostain analogues work for acromegaly?
Inhibits GH release
102
Acromegaly Mx
- 1st= trans-sphenoidal resection of pituitary adenoma
if inoperable unsuccessful...
-Somatostatin analogues e.g ocreotide
103
What are some signs of hypothyroidism?
- Dry hair/skin
- Goitre
- Mental slowness
- Ataxia
- Peripheral neuropathy
- Slow/relaxing reflexes
104
What are some signs of hyperthyroidism?
- Tachycardia
- AF
- Goitre
- Palmar erythema
- Brisk reflexes
105
Hashimotos vs Graves antibodies
Graves - anti TSH reception antibodies
Hashimotos - anti TPO antibodies
106
Where does thyroid gland originate from embryologically?
Foramen caecum
107
What are symptoms of neuroglycopenia?
- Coma
- Seizures
- Drowsiness
- Confusion
108
What are causes of hypoglycaemia in non-diabetic patients?
- Liver failure
- Addisons
- Alcohol binging
- Pituitary insufficiency
- Insulin secreting tumour
109
What happens to periods with hypo and hyperthyroidism?
Hypo - heavy periods
Hyper - irregular/no periods
110
Low vit D, low serum calcium, low serum phosphate, raised ALP and raised PTH
Osteomalacia
111
Osteomalacia
Softening of bones 2 to low vit D leading to decreased bone mineral content. (Called rickets in children).
112
Causes of osteomalacia
Vit D def (malabsorption, lack of sunlight, diet); CKD, drug induced (anticonvulsants), inherited, liver cirrhosis, coeliac
113
Features of osteomalacia
Bone pain, bone/muscle tenderness; fractures (femoral neck); proximal myopathy (waddling gait).
114
Osteomalacia Ix
- Bloods
- X-ray: translucent bands (Looser's zones/psudeofractures)
115
Osteomalacia Mx
vit D supplmentation (loading dose initally) and Ca supp if dietary Ca inadequate
116
What is latent autoimmune diabetes of adulthood and maturity onset diabetes of the young?
LADA - Late onset T1DM - usually aged 30-50
MODY - earl onset T2DM - usually under 25
117
What cardiac manifestations can occur with carcinoid syndrome?
- Pulmonary stenosis and tricuspid insufficiency
118
Management of an incidental pituitary mass?
Lab investigations to assess hormone hypersecretion/hypopituitarism
119
What is alcoholic ketoacidosis?
A euglycemic form of ketoacidosis occurring in alcoholics
- When they don't eat and they become malnourished, they start breaking down ketones
- Presents with metabolic acidosis, elevated ketones and normal/low glucose
- Tx with IV saline and thiamine
120
Depression, nausea, constipation, bone pain
Primary hyperparathyroidism
121
Diabetic ketoacidosis?
Cx of DMT1 or be the first presentation of it. Extreme stress may cause patients with DMT2 to develop DKA.
122
DKA pathophysiology?
Caused by uncontrolled lipolysis which results in XS of free fatty acids that are converted to ketone bodies
123
Most common precipitating factors of DKA?
infection, missed insulin doses, MI
124
DKA CP?
- abdo pain
- polyuria, polydipsia, dehydration
- Acetone-smelling (pear drop smelling) breath
- Kussmaul respiration (deep hyperventilation)
125
DKA diagnostic criteria
- glucose >11mmol/l or known DM
- pH <7.3
- bicarb <15mmol/l
- ketones >3mmol/l or urine ketones ++ on dip
126
DKA Mx: fluid replacement?
0.9% sodium chloride initially eg. 1000ml over 1st hour.
127
DKA Mx: insulin?
IV infusion of 0.1unit/kg/hr. Once blood glucose <14 then 10% dextrose infusion started at 125ml/hr in addition to the 0.9% sodium chloride regime
128
DKA Mx: correction of electrolyte disturbances?
KCl may needed to be added to the replacement fluids. Serum K often high on admission but total body K low, K falls following insulin treatment.
129
If the rate of potassium infusion is greater than 20mmol/hr then what may be required?
Cardiac monitoring
130
Example of a DKA fluid replacement regime for pt with systolic BP on admission 90mmHg and over?
0.9% NaCl 1L= 1000ml over 1st hr
0.9% NaCl 1L with KCl= 1000ml over next 2hrs
0.9% NaCl 1L with KCl= 1000ml over next 2hrs
0.9% NaCl 1L with KCl= 1000ml over next 4hrs
0.9% NaCl 1L with KCl= 1000ml over next 4hrs
0.9% NaCl 1L with KCl= 1000ml over next 6hrs
131
Most pts with DKA deplete how many litres?
5-8
132
DKA Mx
- fluid replacement
- insulin
- correction of electrolyte disturbance
- long-acting insulin continued and short-acting stopped
133
Potassium guidelines in DKA?
- >5.5mmol/l (in first 24hrs)= no replacement
- 3.5-5.5= 40mmol/L infusion solution of potassium
- <3.5= senior review
134
What is an important complication of fluid resus in DKA in children?
Cerebral oedema. So use SLOW infusion for children and young adults (18-25yrs).
135
When to start dextrose infusion in DKA?
When blood glucose is <14
136
DKA resolution is defined as what?
- pH >7.3 and
- blood ketones < 0.6 mmol/L and
- bicarbonate > 15.0mmol/L
137
In DKA, ketonaemia and acidosis should have been resolved within...
24hrs. If not get senoir review.
138
What when DKA resolution criteria met?
- if pt eating and drinking then switch to subcut insulin
- review by diabetes specialist nurse prior to discharge
139
Cx of DKA or the treatment?
- gastric stasis
- thromboembolism
- arrhythmias secondary to hyperkalaemia/iatrogenic
- hypokalaemia
- iatrogenic due to incorrect
- fluid therapy: cerebral oedema, hypokalaemia, hypoglycaemia
- acute respiratory distress syndrome
- AKI
140
What do children/young adults need following fluid resus in DKA?
1:1 nursing to monitor neuro-observations, headache, irritability, visual disturbance, focal neurology etc. Usually 4-12hrs following starting Mx. If suspicion: senior review and CT head
141
Vit D deficiency vs CKD as cause of hyperparathyroidism
Vit d - low calcium and phosphate
CKD - low calcium but raised phosphate
142
What differentials for SIADH must be considered
Severe hypothyroidism + adrenal insufficiency
143
What is Klinefelters syndrome?
- 47 XXY
- Tall and slender male with small testes and gynaecomastia
- Low testosterone with raised FSH:LH
- Managed with HRT + regular monitoring for polycythaemia and DEXA scans for bone mineral density
144
Microvascular vs macrovascular complications of diabetes?
Micro - nephropathy, neuropathy, retinopathy
Macro - CVD/Stroke, MI, PVD
145
What is the pathophysiology of DKA?
Insulin deficiency produces glucose production in the liver;
lipolysis also occurs; fatty acids are broken done to form ketone
bodies which produce a metabolic acidosis
146
What should patients taking steroids be made aware of?
- carry steroid card
- medic alert bracelet
- know how to change dose for sick days
- carry emergency IM hydrocortisone
147
What sensation will be affected first in diabetic neuropathy?
Vibration
148
What findings may be present with diabetic neuropathy on feet?
- Joint deformity
- Painless ulcer
- Diminished reflexes
149
Vomiting in poorly controlled diabetic patient?
Think gastroparesis
150
carpal tunnel syndrome can be associated with what?
Acromegaly
151
What is the most common complication of thyroid eye disease?
Exposure keratopathy
152
What is the management of de Quervains thyroitidits?
Conservative with analgesia. If severe then steroids.
153
What is the most common cause of Cushings syndrome?
Pituitary tumour secreting ACTH (Cushings disease)
154
What can cause low HbA1c?
Sickle cell/G6PD
Hereditary spherocytosis
Haemodialysis
155
Splenectomy can cause what?
Raised Hba1c
156
What is the key parameter to monitor in HHS?
Serum osmolality
157
How to differentiate between unilateral and bilateral sources of aldosterone excess?
High res CT
If normal, adrenal venous sampling
158
Moderate-severe aortic stenosis is a C/I to what?
ACE inhibitors
159
hypertension, hypokalaemia, and metabolic alkalosis
Conn's syndrome
160
What is Conn's?
Primary hyperaldosteronism
161
Causes of Conn's?
- bilateral idiopathic adrenal hyperplasia: (70%)
- adrenal adenoma
- unilateral hyperplasia
- familial hyperaldosteronism
- adrenal carcinoma
162
Features of Conn's?
HTN, hypokalaemia and metabolic alkalosis
163
Conn's Ix?
- 1st: plasma aldosterone/renin ratio= high aldosterone levels, low renin levels (negative feedback due to sodium retention from aldosterone)
- Then CT abdo and adrenal vein sampling: uni adenoma or bilateral hyperplasia
164
What patient's should be screened for Conn's?
- hypertension with hypokalemia
- treatment-resistant hypertension
165
Management of myoxedemic coma?
Thyroxine + Hydrocortisone
166
Conn's Mx?
- laparoscopic adrenalectomy= adrenal adenoma
- aldosterone antagonist e.g. spironolactone= bilateral adrenocortical hyperplasia
167
Management of thyroid storm?
Beta blockers, propylthiouracil and hydrocortisone
168
How should HHS fluids be given?
Slow infusion
169
Which diabetic medication is approved in CKD?
DPP inhibitors
170
What enzyme is deficient in congenital adrenal hyperplasia?
21-hydroxylase
171
What serum marker is raised in CAH?
17-OH progesterone
172
How does CAH present?
- Ambiguous genitalia
- Acne
- Hirsutism
- Delayed puberty
173
How is CAH managed?
- Glucocorticoid (hydrocortisone) and mineralocorticoid (fludrocortisone) replacement
174
If patients are asymptomatic for DM, what do you need?
2 abnormal readings
175
What are side effects of gliotazones?
- Weight gain
- Increased risk of fractures
- Fluid retention
176
Iron tablets/calcium carbonate tablets can have what effect?
Reduced absorption of levothyroxine -> give 4 hours apart
177
How does Cushing's disease present on dex suppression test?
ACTH and cortisol suppressed
178
What time gap should be kept when titrating metformin doses?
1 week
179
Which cancer is Hashimotos thyroiditis associated with?
MALT lymphoma
180
Thyrotoxicosis can lead to what?
high output cardiac failure
181
When should treatment with statins be discontinued?
If serum transaminase concentrations rise to 3 times the upper limit of reference ranges
182
Why does Cushing's cause tanned appearance?
ACTH has a stimulatory effect on the melanocytes due to affinity for the MSH receptor
183
Why does impaired hypoglycaemia awareness occur?
neuropathy of parts of the autonomous nervous system
184
Management of subclinical hypothyroidism
TSH > 10 - Consider thyroxine if this is present on 2 separate occasions atleast 3 months apart
TSH 5.5-10 - Consider 6 months of thyroxine if <65 and there are symptoms of hypothyroidism
If asymptomatic/older - watch and wait
185
What do each of the zones of the adrenals produce?
Zona glomerulosa - Mineralocorticoids - Aldosterone
Zona fasciculata - Glucocorticoids - Cortisol
Zona reticularis - Androgens
Medulla - Adrenaline/Noradrenaline
186
hyperkalaemic, hyponatraemic, hypoglycaemic metabolic acidosis
Adrenal Crisis - Addisons
187
How quickly should ketones fall in DKA?
Atleast 0.5 per hour
188
What are primary causes of hypogonadism?
- Trauma
- Mumps
- Iatrogenic
- Klinefelter's syndrome
189
What is the most common thyroid cancer?
- Papillary
190
What is the management of non adrenal adenoma hyperaldosteronism?
Spironolactone
191
Which cells of pancreas are affected in diabetes?
Beta pancreatic islet cells
192
What genetic mutations might T1DM have?
HLA-DR3/4
193
What time should serum cortisol be taken?
9am
194
Treatment of choice for toxic multinodular goitre?
Radioactive iodine
195
Osteoporosis in a man?
Check testosterone
196
What is the management of Addisonian crisis?
- Hydrocortisone
- 1L Saline
197
How do DPP-4 inhibitors work?
Increase incretin levels by reducing their peripheral breakdown
198
How should the dose of hydrocortisone be taken in someone with Addisons?
Majority in first half of the day
199
What should be corrected before giving bisphosphonates?
Hypocalcaemia
Vit D deficiency
200
Patient >75 with fragility fracture?
Start bisphosphonate without needing to do DEXA
201
What dose of glucose gel should be given to a patient with a low blood sugar?
10-20g
202
Which HTN drug an cause sexual dysfunction?
Thiazide-like diuretics e.g indapamide
203
How long should metformin be discontinued for after CT with contrast?
48 hours
204
In primary prevention of CVD, what should the non-HDL cholesterol reduce by?
>40% within the first 3 months
205
What should be done after treatment with bisphosphonates for 5 years?
Repeat DEXA and FRAX and stop if score <-2.5
206
Which diabetes medication is linked to Fournier's gangrene (necrotising fasciitis of the genitals)?
SGLT-2 inhibitors
207
What is the investigation of choice for suspected insulinoma?
72 hour fast
208
Ferrous sulphate can interact with what?
Levothyroxine
209
Management of hyperglycaemia in someone who has started enteral feeding?
Insulin
210
Management of steroid induced diabetes?
Sulfonylureas e.g. gliclazide
211
Primary amenorrhoea?
Failure to establish mentruation by 15yrs but normal secondary sexual characteristics; or by 13yrs with no characteristics
212
Secondary amenorrhoea?
Cessation of menstruation for 3-6m in women with normal regular menses or 6-12m in women with previous oligomenorrhoea
213
Causes of primary amenorrhoea
Gonadal dysgenesis eg. Turner's (common); testicular feminisation; congenital malformations of genital tract; functional hypothalamic amenorrhea eg. 2 to anorexia; imperforate hymen; congenital adrenal hyperplasia
214
Causes of secondary amenorrhoea (after excluding pregnancy)
hypothalamic amenorrhoea eg. 2 to stress, XS exercise; PCOS; hyperprolactinaemia; premature ovarian failure; thyrotoxicosis; Sheehan's; Asherman's
215
Amenorrhoea Ix
- urinary or serum bHCG
- FBC, U&E, coeliac screen, TFTs
- prolactin
- oestradiol
- androgen levels (raised in PCOS)
- gonadotrophins= low means hypothalamic cause, raised suggest ovarian problem (premature ovarian failure) or gonadal dysgenesis eg. Turner's
216
Amenorrhoea Mx
-TUC
- Primary: with primary ovarian insufficiency due to gonadal dysgenesis eg. Turner's then HRT eg. to prevent osteoporosis ect.
217
What is gynaecomastia?
Abnormal amount of breast tissue in males caused usually by increased oestrogen:androgen ratio.
218
Causes of gynaecomastia?
- physiological: normal in puberty
- syndromes with androgen deficiency: Kallman's, Klinefelter's
- testicular failure: e.g. mumps
- liver disease
- testicular cancer e.g. seminoma secreting hCG
- ectopic tumour secretion
- hyperthyroidism
- haemodialysis
- drugs
219
Drug causes of gynaecomastia?
- spironolactone (most common)
- cimetidine
- digoxin
- cannabis
- finasteride
- GnRH agonists e.g. goserelin, buserelin
- oestrogens, anabolic steroids
220
Very rare drug causes of gynaecomastia?
- tricyclics
- isoniazid
- calcium channel blockers
- heroin
- busulfan
- methyldopa
221
What is dysmenorrhoea?
XS pain during menstrual period. Primary and secondary.
222
Primary dysmenorrhoea?
No underlying pelvic pathology. Partially due to EX endometrial prostaglandin production.
223
Primary dysmenorrhoea features?
up to 50% women, usually within 1-2yrs of menarche.
- pain just before or within few hrs or period starting
- usually lasts 72hrs and improves as menses progress
- suprapubic cramping pains which may radiate to back or down thigh
- vomiting, nausea, fatigue, dizziness
224
Primary dysmenorrhoea Mx
- NSAIDs eg. ibuprofen and mefenamic acid= inhibit prostaglandin production
- 2nd: COCP
225
Secondary dysmenorrhoea?
Result of underlying pathology and develops many yrs after menarche
226
Secondary dysmenorrhoea feature?
Pain usually starts 3-4 days before onset of period
- dyspareunia
- not really related to menstruation but this exacerbates pain
227
Causes of secondary dysmenorrhoea?
Endometriosis, adenomyosis, PID, copper coil, fibroids.
228
Mx for secondary dysmenorrhoea
Refer to gynaecology for investigation
229
Red flags for dysmenorrhoea
- +ve preg test and vag bleeding
- ascites/pelvic/abdo mass
- abnormal cervix on pelvic exam
- persistent intermenstrual or postcoital bleeding with features of PID
230
What is Addison's disease?
Primary adrenal insufficiency. Autoimmune destruction of adrenal glands. Most common cause of hypoadrenalism (80% cases).
231
What does Addison's result in?
Reduced cortisol (glucocorticoid) and aldosterone (mineralocorticoid) being produced.
232
Addison's CP?
- lethargy, weakness, weight loss, N&V
- salt craving
- hyperpigmentation (esp palmar creases)
- vitilligo
- loss of pubic hair in women
- hypotension
hypoglycaemia
- may be hyponatraemia and hypokalaemia
233
When should Addison's be considered?
- persistent non-specific symptoms (of addisons)
- hypothyroidism if symptoms worsen when thyroxine is started
- DMT1 with recurrent unexplained hypoglycaemic episodes
- other autoimmune conditions
- low Na or high K levels
234
Addisonian crisis CP
hypotension, hypovolaemic shock, acute abdo pain, vomiting, reduced consciousness
235
Addison's Ix?
- Inital:
* 8-9am serum cortisol
* urea & electrolytes.
- GOLD (confirm diagnosis): Synacthen test (adrenocorticotrophic hormone simulation)
236
What do the 9am serum cortisol levels mean?
- <100nanomol then admit to hospital as adrenal insuff highly likely.
- 100-500 then refer to endo for Ix
237
What autoantibodies may be common in Addison's?
Adrenal cortex autoantibodies or 21-hydroxylase antibodies
238
Normal response to ACTH simulation test (Synacthen test)?
Cortisol levels increase to more than 500nanomol/L after 30-60mins.
If adrenal insfuficiency: serum cortisol levels don't repsond to tetracosactide but adrenal cortex already receiving max stimulation from endogenous ACTH.
239
Addison's Mx?
Hydrocortisone for glucocorticoid replacement and fludrocortisone for mineralcorticoid replacement.
240
Important information to tell someone who has Addison's?
- INCREASE corticosteroid during physical stress eg. illness, injury or surgery to prevent adrenal crisis: DOUBLE glucocortiocid and keep fludrocortisone dose same
- Recognise symptoms of adrenal crisis
- Carry steroid emergency card
241
Causes of Addisonian crisis?
Current illness or stress.
242
Mx of Addisonian crisis
IM or IV hydrocortisone and admit to hospital
243
Primary vs secondary adrenal insufficeny?
- Primary (Addison's)= adrenal glands don't make enough cortisol and aldosterone
- Secondary= pituitary doesn't make enough ACTH
244
What is ACTH (adrenocorticotropic hormone)?
Produced by pituitary gland that regulates cortisol and androgen production. When released it triggers adrenal glands to produce C and A.
245
Causes of primary hypoadrenalism (Addison's)?
- Autoimmune (most)
- congenital adrenal hyperplasia
- TB
- Metastases eg. bronchial carcinoma
- meningococcal septicaemia (Waterhouse-Friderichsen syndrome)
- HIV
- antiphospholipid syndrome
246
Causes of secondary hypoadrenalism?
- pituitary disorders eg. tumours, irradiation, infiltration
- long term administration of corticosteroids
247
Diabetes insipidus (DI)?
Decreased secretion of antidiuretic hormone (ADH) from pituitary (cranial DI) or insensitivity to ADH (nephrogenic DI).
248
Causes of cranial DI
- idiopathic
- post head injury
- pituitary surgery
- craniopharyngiomas
- infiltrative= sarcoidosis, histiocytosis X
- DIDMOAD (DM, Optic Atrophy and Deafness- Wolfram's syndrome)
- haemochromatosis
249
Causes of nephrogenic DI
- genetic
- electrolytes= hypercalcaemia, hypokalaemia
- lithium
- demeclocycline
- tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis
250
Genetic causes of nephrogenic DI
- affects the vasopressin (ADH) receptor
- or mutation in gene that encodes the aquaporin 2 channel
251
How does lithium cause nephrogenic DI?
Desensitised the kidney's ability to respond to ADH in collecting ducts
252
CP of DI
polydipsia and polyuria
253
DI Ix
- high plasma osmolality, low urine osmolality
- urine osmolality of >700mOsm/kg excludes diabetes insipidus
- water deprivation test
254
DI Mx: nephrogenic
thiazides and low salt/protein diet
255
DI Mx: crainial
Desmopressin
256
What is the water deprivation test (desmopressin stimulation test)?
Used to evaluate pts who have polydipsia.
1. prevent pt drinking water 8hrs before test
2. measure urine osmolality
3. if urine osm low, then synthetic ADH (Desmopressin) is given
4. re-measure urine osm 2-4hrs later
257
Water deprivation test: primary polydipsia
- urine osm after water deprivation= high
- urine osm after desmopressin= N/A
rules out DI
258
Water deprivation test: cranial DI
- urine osm after water deprivation= low
- urine osm after desmopressin= high
pt lacks ADH, kidneys still capable of responding to ADH. Initially urine osm low as continues to be diluted by XS water lost in urine. After des given, kidneys respond by reabsoring water and concentrating water so urine osm high.
259
Water deprivation test: nephrogenic DI
- urine osm after water deprivation= low
- urine osm after desmopressin= low
pt unable to respond to ADH so both low.
260
Hyperosmolar hyperglycaemic state (HHS)?
Medical emergency, usually elderly with DMT2 and up to 20% mortality.
261
What does HHS result in?
Hyperglycaemia results in osmotic diuresis, severe dehydration and electrolyte def.
262
HHS pathophysiology
hyperglycaemia → ↑ serum osmolality → osmotic diuresis → severe volume depletion
263
HHS clinical presentation
- comes on over many days (DKA hrs) so dehydration and metabolic distrubances more extreme
- Cx of volume loss= polyuria, polydipsia, dehydration
- systemic= lethargy, N&V
- neurological= altered consciousness, focal neuro deficits
- haematological= hypervidcosity (MI, stroke, peripheral arterial thrombosis)
264
What is typically seen in HHS for diagnosis?
- hypovolaemia
- hyperglycaemia= >30
- raised serum osmolarity= >320mosmol/kg
- no hyperketonaemis= <3
- no acidosis= bicarb >15 or pH >7.3 (can occur due to lactic acidosis or renal impairment however)
265
How to calculate serum osmolarity in HHS?
2 * Na+ + glucose + urea
266
HHS Mx
- fluid replacement
- insulin= should not be given unless blood glucose stops falling while giving IV fluids
- VTE prophylaxis
267
HHS Mx: fluid replacement?
- fluid loss estim 100-200ml/kg
- IV 0.9% sodium chloride
- 0.5-1L/hr
- Monitor K+ levels and add to fluids if needed
268
HHS Cx?
Vascular due to hyperviscosity eg. MI, stroke
269
When do most children achieve day and night continence by?
3-4yrs
270
Enuresis?
Involuntary discharge of urine by day or night or both in child 5yrs+, in absence of congenital or acquired defects of NS or urinary tract.
271
Nocturnal enuresis?
- Primary= never achieved sustained continence at night
- Secondary= after child has been previously dry at night for >6m
272
Causes of primary nocturnal enuresis?
sleep arousal difficulties, polyuria, bladder dysfunction
273
Causes of secondary nocturnal enuresis?
diabetes, UTI, constipation, psychological problems
274
Causes of primary nocturnal enuresis with daytime symptoms?
overactive bladder, congenital malformations, neuro disorders, UTI, chronic constipation
275
RFs for nocturnal enuresis
FHx, male, delay in attaining bladder control, obesity, ADHD, autism, anxiety
276
Important points to ask in nocturnal enuresis history?
- daytime symptoms?
- previously dry at night without assistance for 6m?
277
Nocturnal enuresis Mx?
- advice: lifting and waking, fluid intake, toilet before bed. If infrequent (<2 times week) or <5yrs then reassure that usually resolves without Mx and wait-and-see approach
- 1st= enuresis alarm AND positive reward system (eg. star charts) for agreed behaviour eg. using toilet before bed rather than dry night
- 2nd= desmopressin for short term eg. sleepover or if alarm ineffective.
278
Common (>1 in 10) causes of polyuria
- diuretics, caffeine and alcohol
- DM
- lithium
- HF
279
Infrequent (1 in 100) causes of polyuria
- hypercalcaemia
- hyperthyroidism
280
Rare (1 in 1000) causes of polyuria
- chronic renal failure
- primary polydipsia
- hypokalaemia
281
Very rare (<1 in 10000) causes of polyuria
Diabetes insipidus
282
Hyperthyroidism?
Pathologically increased thyroid hormone production and secretion by thyroid gland
283
Thyrotoxicosis?
Clinical manifestation of XS thyroid hormone due to any cause, incl. hyperthyroidism
284
Primary hyperthyroidism?
When thyrotoxicosis is caused by abnormality of thyroid gland eg. Graves' or a nodular goitre
285
Pathophysiology of primary hyperthyroidism?
When thyroid-stimulating hormone (TSH) is suppressed below normal reference range and free thyroxine (FT4) and/or free triiodothyronine (FT3) concs are high
286
Pathophysiology of subclinical hyperthyroidism
TSH low and T4/T3 normal
287
Thyrotoxicosis without hyperthyroidism?
Thyrotoxicosis without thyroid gland overacitivity, normally transiet due to thyroiditis or XS levothyroxine.
288
Cx of hyperthyroidism
thyrotoxic crisis, Graves orbitopathy, compression symptoms from large goitre, AF, HF
289
Causes of primary, secondary and tertiary hyperthyroidism?
1= thyroid pathology eg. Graves, thyroid adenoma, toxic multinodular goitre
2= pituitary pathology eg. XS iodine
3= hypothalmic
290
Hyperthyroidism CP
T.remor
H.eart rate increase
Y.awning
R.estlessness
O.ligomenorrhoea
I.rritability
D.iarrhoea
I.ntolerance to heat
S.weating
M.uscle wasting
PAINLESS GOITRE, anxiety, WEIGHT LOSS, sinus tachy, features of graves
291
Graves' disease CP
- orbitopathy: XS eye watering, eyelid retraction or lid lag, proptosis, double vision, changes in visual acuity or colour vision
- non-pitting pretibial myxoedema
- thyroid bruit
292
DeQuervains?
After upper resp infection. Thyroid PAINFUL
293
Hyperthyroidism Ix?
TFTs:
- Primary= TSH low, T3 & T4 high
- Subclinical= TSH low, T3 & T4 normal
- Secondary= TSH high, T3 & T4 high
- Repeat TFTs after 3m to confirm
- TRAb (TSH receptor antibodies) if suspect Graves
- ESR & CRP ?thyroiditis
294
Hyperthyroidism Mx
- Beta blocker for andrenergic symptoms
- + Carbimazole
- definitive Mx: radioactive iodine or thyroid surgery
295
Monitoring of carbimazole?
FBC and LFTs before starting
296
Graves' Mx
Sunglasses, IV methylprednisolone, surgical decompression
297
Hypothyroidism?
Thyroid hormone (thyroxine T4 and tri-iodothyronine T3 def)
298
Primary hypothyroidism (overt)
TSH high, T3 & T4 low
299
Secondary hypothyroidism
TSH low/normal, T3 & T4 low
300
Subclinical hypothyroidism
TSH high, T3 & T4 normal
301
Tertiary hypothyroidism
TSH low, T3 & T4 low, TRH low
302
Causes of primary hypothyroidism
- autoimmune thyroiditis (Hashimotos)
- iodine def
- post-ablative therapy or surgery
- drugs
- Subacute thyroiditis (de Quervain's)
- transient thryoiditis
- thyroid infiltrative disorders
303
What drugs can cause hypothyroidism?
Amiodarone, lithium, carbimazole
304
Cause of secondary hypothyroidism
Pituitary eg. tumour. Associated with Down's, Turner's and coeliac.
305
Causes of teritary hypothyroidism
Hypothalamic
306
Cx of hypothyroidism
dyslipidaemia, metabolic syndrome, CHD, stroke, HF, neuro and cognitive impairments, adverse maternal & fetal outcomes in preg
307
Hypothyroidism CP
B.readycardia
R.eflexes relax slowly
A.taxia
D.ry thin hair and skin
Y.awning
C.old intolerance
A.scites
R.ound puffy face
D.epression
I.mmobile ileus (constipation)
C.ongestive HF
WEIGHT GAIN, PAINLESS GOITRE
308
Hypothyroidism Ix
- TFTs
- TPOAb (thyroid peroxidase antibodies) if ?autoimmune cause
- FBC and B12: pernicious anaemia
- HbA1c
- coeliac serology
serum lipids
309
Hypothyroidism Mx
Levothyroxine (T4).
Refer to endo if pregnant, postpartum planning pregnancy or already diagnosed with postpartum thyroiditis.
310
Levothyroxine dose?
50-100mcg od starting.
If >50yrs, severe hypothy or IHD then start inital at 25mcg od then titrate slowly.
311
Therapeutic goal for levothyroxine?
TSH 0.5-2.5mU/l
312
Following change in levothyroxine dose, when should TFTs be checked?
After 8-12w
313
Levothyroxine S/E?
hyperthyroidism, reduced BMD, worsening angina, AF
314
Levothyroxine interactions?
Iron, calcium carbonate.
Absorption of thyroxine reduced so give 4hrs apart
315
Hashimoto's thyroiditis: hashitoxicosis?
Transient thyrotoxic state
316
Diabetes mellitus type 1 and 2 classification?
Fasting plasma glucose >7
Random plasma glucose >11
HbA1c >48
317
DMT1 cause?
Absolute insulin def resulting from autoimmune destruction of insulin producing pancreatic beta cells of the islets of Langerhans.
318
Cx of DMT1: microvascular
retinopathy, nephropathy, neuropathy
319
Cx of DMT1: macrovascular
MI, stroke, PAD
320
Cx of DMT1: metabolic
DKA, hypoglycaemia (<3.5)
321
Other Cx of DMT1?
Depressions, eating disorders, risk of other autoimmune conditions eg. thyroid, coeliac, pernicious anaemia, addison's
322
How do pts with DMT1 typically present?
Early life, unwell- possibly in DKA
323
When should you suspect DMT1 in children/young adult?
hyperglycaemia +
polyuria, polydipsia, weight loss, XS tiredness
324
DMT1 clinical diagnosis?
Hyperglycaemia + 1 or more:
- ketosis
- weight loss
- <50yrs (>rarer)
- BMI <25 (>rarer)
- FHx or personal history of autoimmune disease
325
DMT1 Ix?
- clinical + urine dip for glucose and ketones + fasting and random glucose + HbA1c
- Can do c-peptide levels= typically low
- diabetes specific autoantibodies= distinguish between T1 & T2 eg. anti-GAD in T1
326
DMT1 Mx
Subcut insulin
327
DMT2 cause?
Persistent hyperglycaemia caused by combination of deficient insulin secretion and resistance to the action of insulin.
328
DMT2 RFs?
obesity, inactivity, diet, FHx, Asian, African, Afro-Caribbean, long-term corticosteroids, Hx gestational diabetes
329
DMT2 Cx
Same as T1
330
When to suspect DMT2?
- persistent hyperglycaemia
- polydipsia, polyuria, weight loss, tiredness, enuresis, impaired growth in children, acanthosis nigricans (suggesting insulin resisitance)
331
Mx of DMT2
- Individualised care plan
- Education, support, advice in lifestyle
- Screening for complications
- Lifestyle Mx
- Medication if lifestyle not sufficient
332
DMT2 antidiabetic medication?
1st: metformin standard release (not at CVD risk) or metformin standard relase + SGLT2 inhibitor (risk of CVD.
- if GI disturbance with metformin then switch to metformin modified release
2nd: + sulfonylurea, pioglitazone or DPP-4 inhibitor ('gliptin')
3rd: dual therapy not worked= consider insulin based therapy (with or without other drugs). Can also try triple therapy= + sulfonylurea, pigoglitazone or DPP-4 in.
4th: triple therapy not working with metformin + 2 other drugs, switch one of the drugs to GLP-1 mimetri eg. exenatide (SC)
333
DMT2: how often should HbA1c be measured?
3-6m until stable then 6mthly
334
DMT2 'sick day rules' advice?
Stop medication except insulin
335
Diabetes Ix to check blood glucose?
- finger prick
- fasting or random blood glucose
- HbA1c
- oral glucose tolerance test
336
Side effects of insulin?
Hypoglycaemia, weight gain, lipodystrophy
337
Insulin mechanism of action
direct replacement for endogenous insulin
338
Metformin mechanism of action
increases insulin sensitivity; decreases hepatic gluconeogenesis
339
Metformin side effects
GI upset, lactic acidosis. Can't be used in pts with eGFR <30
340
Sulfonylureas mechanism of action?
Stimulate pancreatic beta cells to secrete insulin
341
Sulfonylureas side effects?
Hypoglycaemia, weight gain, hyponatraemia, SIADH
342
DPP-4 inhibitors (gliptins) mechanism of action?
Increase incretin levels which inhibit glucagon secretion
343
DPP-4 inhibitors (gliptins) side effects?
Increased risk of pancreatitis
344
Thiazolidinediones mechanism of action?
Activate PPAR-gamma receptor in adipocytes to promoite adipogenesis and fatty acid uptake
345
Example of Thiazolidinediones?
pioglitazone
346
Thiazolidinediones side effects?
Weight gain, fluid retention, fractures
347
SGLT-2 inhibitors (-gliflozins) mechanism of action?
reversibly inhibit sodium-glucose co-transporter 2 (SGLT-2) in the renal proximal convoluted tubule to reduce glucose reabsorption and increase urinary glucose excretion.
348
SGLT-2 inhibitors (-gliflozins) side effects?
UTI, weight loss, increased risk of lower-limb amputation so monitor feet
349
SGLT-2 inhibitors (-gliflozins) example?
canagliflozin, dapagliflozin
350
GLP-1 agonists (-tides) mechanism of action?
Incretin mimetic which inhibits glucagon secretion
351
GLP-1 agonists (-tides) side effects?
N&V, pancreatitis, weight loss
352
Prediabetes?
This term is used for patients who don't yet meet the criteria for a formal diagnosis of T2DM to be made but are likely to develop the condition over the next few years. They, therefore, require closer monitoring and lifestyle interventions such as weight loss
353
Gestational diabetes?
Some pregnant develop raised glucose levels during pregnancy. This is important to detect as untreated it may lead to adverse outcomes for the mother and baby
354
Maturity onset diabetes of the young (MODY)?
A group of inherited genetic disorders affecting the production of insulin. Results in younger patients developing symptoms similar to those with T2DM, i.e. asymptomatic hyperglycaemia with progression to more severe complications such as diabetic ketoacidosis
355
Latent autoimmune diabetes of adults (LADA)?
The majority of patients with autoimmune-related diabetes present younger in life. There are however a small group of patients who develop such problems later in life. These patients are often misdiagnosed as having T2DM
356
What else can cause diabetes?
Any pathological process which damages the insulin-producing cells of the pancreas may cause diabetes to develop. eg. chronic pancreatitis and haemochromatosis.
357
What drugs can cause raised blood glucose levels?
Glucocorticoids
358
BP target for diabetics?
140/90mmHg
359
What should be avoided in diabetics with uncomplicated HTN as they may cause insulin resistance/impair insulin secretion?
Beta blockers
360
DMT1 blood glucose targets?
5-7 mmol/l on waking and
4-7 mmol/l before meals at other times of the day
361
DMT1 types of insulin?
- Multiple daily injection basal-bolus insulin regimens
eg. twice-daily insulin detemir
- Rapid-acting insulin analogues injected before meals
362
DMT2: what should be done before starting a patient with CVD risk of SGLT-2 inhibitors?
Metformin should be esablished and titrated up before starting.
363
DMT2: when should a SGLT-2 inhibitor be started?
Start SGLT-2 at any point if pt develops CVD, QRISK >10 or HF.
364
If triple therapy not tolerated then when should you consider switching one of the drugs for GLP-1 mimetic?
- BMI ≥ 35 kg/m² and specific psychological or other medical problems associated with obesity or
- BMI < 35 kg/m² and for whom insulin therapy would have significant occupational implications or weight loss would benefit other significant obesity-related comorbidities
- only continue if there is a reduction of at least 11 mmol/mol [1.0%] in HbA1c and a weight loss of at least 3% of initial body weight in 6 months
365
Advice to give muslims who are diabetic during Ramadan?
- eat meal containing long-acting carbs at Suhoor
- check blood glucose levels
- if taking metformin, split to 1/3 dose at Suhoor and 2/3 dose at Iftar
- take once daily sulfonylureas at Iftar
366
Why should a patient on insulin not stop it if they are sick?
risk of DKA
367
Presentation of diabetic foot?
- neuropathy
- ischaemia: absent foot pulses, reduced ABPI, intermittent claudication
- ulceration, Charcot's arthropathy, cellulitis
368
How often to screen for diabetic foot?
Anuually. If moderate or high risk (problems other than simple calluses) then follow up regularly at diabetic foot centre
369
Contraindications to metformin?
CKD (eGFR <30); recent MI, sepsis; having iodine-containing x-ray contrast media; alcohol abuse
370
2 main types of impaired glucose regulation?
- impaired fasting glucose (IFG): due to hepatic insulin resistance
- impaired glucose tolerance (IGT): due to muscle insulin resistance
371
What implies impaired fasting gluocse?
a fasting glucose greater than or equal to 6.1 but less than 7.0 mmol/l
372
What is impaired glucose tolerance defined as?
fasting plasma glucose less than 7.0 mmol/l and OGTT 2-hour value greater than or equal to 7.8 mmol/l but less than 11.1 mmol/l
373
What should people with impaired fasting glucose be offered?
oral glucose tolerance test to rule out a diagnosis of diabetes. A result below 11.1 mmol/l but above 7.8 mmol/l indicates that the person doesn't have diabetes but does have IGT
374
What is diabetic nephropathy?
Commonest cause of end-stage renal disease in world; 33% pts with DMT1 have it by 40yrs
375
Pathophysiology of diabetic nephropathy?
- Changes to haemodynamics of glomerulus, leads to increased glomerular capillary pressure.
- Non-enzyme glycosylation of basement membrane
376
Histological changes in diabetic nephropathy?
BM thickening, capillary obliteration, mesangial widening. Nodular hyaline areas develop in glomuli-Kimmelstiel-Wilson nodules.
377
Modifiable RFs for diabetic nephropathy?
Hypertension
Hyperlipidaemia
Smoking
Poor glycaemic control
Raised dietary protein
378
Non-modifiable RFs for diabtic nephropathy?
Male sex
Duration of diabetes
Genetic predisposition (e.g. ACE gene polymorphisms)
379
Screening for diabetic nephropathy how often?
Annually
380
How do you screen for diabetic nephropathy?
Urinary albumin:creatinine ratio (ACR), early morning specimin.
ACR>2.5= microalbuminuria
381
Diabetic nephropathy Mx
- dietry protein restriction
- tight glycaemic control
- BP control (aim <130/80)
- ACE in or ARB
- control dyslipidaemia eg. statins
382
Diabetic nephropathy- when to start ACE or ARB?
if urinary ACR 3+
DONT use dual therapy.
383
How many stages of diabetic nephropathy?
5
384
Diabetic nephropathy stage 1?
- hyperfiltration: increase in GFR
- may be reversible
385
Diabetic nephropathy stage 2 (silent or latent phase)
- most don't develop microalbuminuria for 10yrs
- GFR remains elevated
386
Diabetic nephropathy stage 3 (incipient nephropathy)
- microalbuminuria (albumin excretion 30-300mg/day, dipstick neg)
387
Diabetic nephropathy stage 4 (overt nephropathy)
- persistent proteinuria (albumin excretion >300, dip +ve)
- HTN present
- Histology= diffuse glomerulosclerosis and focal glomerulosclerosis (Kimmelstiel-Wilson nodules)
388
Diabetic nephropathy stage 5
- end stage renal disease, GFR <10
- renal replacement therapy needed
389
Diabetic nephropathy in DMT1 vs DMT2
DMT2 same stages as T1 but may progress at different timescale- quicker to later stag
390
Diabetic neuropathy?
Sensory loss NOT motor loss
391
Diabetic neuropathy: peripheral neuropathy typical sensory loss pattern?
Glove and stocking distribution.
Lower longs affected 1st due to length of sensory neurone affecting this area.
Painful neuropathy is common.
392
Diabetic neuropathy Mx
- pain Mx clinics
- 1st: amitriptyline, duloxetine, gabapentin or pregabalin
- 2nd: + another
- localised neuropathic pain eg. post-herpetic neuralgia= topical capsaicin
393
Diabetic neuropathy: what can be used as 'rescue therapy' for exacerbations of neuropathic pain?
Tramadol
394
Diabetic neuropathy: 2 types?
Peripheral neuropathy and GI autonomic neuropathy
395
Diabetic GI autonomic neuropathy?
- gastroparesis
- chronic diarrhoea (at night)
- GORD
396
Diabetic GI autonomic neuropathy: gastroparesis?
- secondary to autonomic neuropathy
- CP: erratic blood glucose control, bloating and vomiting
- Mx: metoclopramide, domperidone or erythromycin (prokinetics)
397
Diabetic GI autonomic neuropathy: GORD caused by what?
decreased lower oesophageal sphincter pressure
398
When does a patient need primary prevention for hyperlipidaemia?
QRISK= 10+
DMT1
CKD is eGFR <60
Most people over 60yrs ideally
399
Primary prevention for hyperlipdaemia?
Atorvastatin 20mg od. If not fallen by >=40% then titrate up to 80
400
Secondary prevention for hyperlipidaemia (known IHD, CVD, PAD)?
Atorvastatin 80mg od
401
QRISK may underestimate CVD risk in what populations?
- pts treated for HIV
- serious mental health problems
- meds causing dyslipidaemia: antipsychotics, corticosteroids, immunosuppressants
- autoimmune disorders/systemic inflam disorders eg. SLE
402
When to consider possibility of familial hypercholesterolaemia?
- total cholestrol >7.5
- personal or FHx of premature CHD (event before 60yrs in person or first degree relative)
403
Atorvastatin 20mg should be offered to T1 diabetics who are...
- >40yrs
- diabetes >10yrs
- established nephropathy
- or other CVD RFs
404
In CKD what should be done before increasing a dose of atorvastatin?
Consult renal specialist
405
Follow up after starting pt on a statin?
at 3m:
- repeat full lipid profile
406
When following a pt up, what if the non-HDL cholesterol has not fallen by at least 40%?
Talk about concordance and lifestyle changes with pt. Consider increasing atorvastatin up to 80mg.
407
What is xanthelasma?
Yellowish papules and plaques commonly seen on eyelid
408
What is xanthelasma appearance caused by?
Localised accumulation of lipid deposits. Also seen in pts without lipid abnormalities
409
Mx of exanthelasma?
Surgical excision, topical trichloroacetic acid, laser therapy or electrodesiccation
410
Palmar xanthoma?
- remnant hyperlipidaemia
- may less commonly be seen in familial hypercholesterolaemia
411
Eruptive xanthoma?
Due to high triglyceride levels and present as multiple red/yellow vesicles on extensor surfaces (elbows, knees)
412
Causes of eruptive xanthoma?
- familial hypertriglycerdaemia
- lipoprotein lipase def
413
Tendon xanthoma, tuberous xanthoma and xanthelasma?
- familial
- hypercholesterolaemia
remnant hyperlipidaemia
414
Mechanism of action of statins?
Inhibit action of HMG-CoA reductase (rate limiting enzyme in hepatic cholesterol synthesis)
415
Aim of treatment in secondary prevention (statins)?
LDL-C level of 2.0 mmol per litre or less, or non-HDL-C levels of 2.6 mmol per litre or less
416
Aim of treatment in primary prevention (statins)?
greater than 40% reduction in non-HDL-C levels.
417
Before starting lipid modification therapy, what baseline bloods should be performed?
- non-fasting lipid profile
- LFTs
- Renal function
- HbA1c
- creatine kinase
- TFTs
418
Adverse effects of statins?
- myopathy: myalgia, myositis, rhabdomyolysis
- liver impairment (check LFTs 3m and 12m)
- increase risk intracerebral haemorrhage
419
Statin contraindications
- pregnancy
- macrolides (erythromycin, clarithromycin)
420
When should statins be taken?
At night- majority of cholestrol synthesis takes place here.
421
Causes of hypoglycaemia
- insulinoma
- self administration fo insulin
- liver failure
- Addison's
- alcohol
-nesidioblastosis (beta cell hyperplasia)
422
What is insulinoma?
Increased ratio of proinsulin to insulin
423
How does alcohol cause hypoglycaemia?
Causes XS insulin secretion.
Affects pancreatic microcirculation → redistribution of pancreatic blood flow from the exocrine into the endocrine parts → increased insulin secretion.
424
Hormonal response to hypoglycaemia?
decrease insulin secretion, increase glucagon secretion. GH and cortisol released but later.
425
Sympathoadrenal response to hypoglycaemia?
increased catecholamine-mediated (adrenergic) and acetylcholine-mediated (cholinergic) neurotransmission in the peripheral autonomic nervous system and CNS
426
Blood glucose conc <3.3mmol/L cause what?
Autonomic symptoms due to release of glucagon and adrenaline
427
Blood glucose conc <2.8 cause what?
neuroglycopenic symptoms due to inadequare glucose supply to the brain
428
CP of pt with blood glucose <3.3?
sweating, shaking, hunger, anxiety, nausea
429
CP of pt with blood glucose <2.8?
weakness, vision changes, confusion, dizziness
430
CP of pt with severe hypoglycaemia?
Convulsion, coma
431
Mx of hypoglycaemia in community?
- oral glucose 10-20g in liquid, gel or tablet form
- or quick acting carb eg. GlucoGel or Dextrogel
- Hypokit may be prescribed (glucagon for IM or SC injection at home)
432
Mx of hypoglycaemia in hospital?
- if pt is alert, then quick acting carb
- unconcious: SC or IM glucagon or IV 20% glucose solution
433
Types of bariatric surgery?
- Primarily restrictive operations
- Primary malabsorptive operations
- Mixed operations
434
Bariatric surgery: types of restrictive operations?
- laparoscopic-adjustable gastric banding (LAGB): fewest Cx but less weight loss
- Sleeve gastrectomy (stomach reduced to 15% of orginial)
- Intragastric balloon (max 6m)
435
Bariatric surgery: example of malabsorptive operation?
biliopancreatic diversion with duodenal switch (if BMI >60)
436
Bariatric surgery: example of mixed operations (restrictive and malabsorptive)?
Roux-en-Y gastric bypass surgery
437
First line bariatric surgery in pts with BMI 30-39kg/m2?
laparoscopic-adjustable gastric banding (LAGB)
438
Underweight BMI
<18.49
439
Normal BMI
18.5-25
440
Overweight BMI
25-30
441
Obese class 1, 2 & 3 BMI
1= 30-35
2= 35-40
3= >40
442
Medical Mx for obesity
Orlistat or liraglutide
443
What is the mechanism of action of Orlistat?
Pancreatic lipase inhibitor
444
Criteria for using orlistat for obesity?
- BMI 30+ or 25+ with RFs
- continued weight loss eg. 5% at 3m
- <1yr use
445
What is Liraglutide?
Glucagon-like-peptide (GLP-1) mimetic used for weight loss and DMT2 Mx. Once daily SC.
446
Criteria for using Lireaglutide for obesity?
BMI 35+
or prediabetic hyperglycameia (HbA1c 42-47)
447
Pituitary adenoma?
Benign tumour of pituitary gland. Common but mainly never found (asymptomatic) or incidental finding).
448
How are pituitary adenomas classified?
Size and hormonal status
449
Microadenoma size?
<1cm
450
Macroadenoma size?
>=1cm
451
Secretory/functioning adenoma?
Produces an XS of a particular hormone
452
Non-secretory/functioning adenoma?
Does not produce hormone to XS
453
Most common type of pituitary adenoma?
Prolactinoma.
Then non-secreting adenomas, then GH-secreting and ACTH-secreting adenomas
454
How do pituitary adenomas typically cause symptoms?
XS hormone, depletion of a hormone, stretching of the dura within/around pituitary fossa (eg. headaches) or compression of the optic chiasm.
455
Examples of pituitary adenoma causing XS hormone?
- Cushing's disease: XS ACTH
- Acromegaly: XS GH
- Amenorrhoea/galactorrhoea: XS prolactin
456
Example of pituitary adenoma causing depletion of a hormone?
due to compression of normal pituitary gland.
Eg. non-functioning tumours: hypopituitarism
457
What CP does a pituitary adenoma compressing the optic chiasm cause?
Bitemporal hemianopia due to crossing nasal fibres
458
What is a pituitary incidentaloma?
When they are incidental finding on neuroimaging eg. microadenoma.
459
Pituitary adenoma Ix?
- pituitary blood profile (GH, prolactin, ACTH, FSH, LSH, TFTs)
- visual field testing
- MRI brain with contrast
460
Pituitary adenoma differential diagnoses?
pituitary hyperplasia
craniopharyngioma
meningioma
brain metastases
lymphoma
hypophysitis
vascular malformation (e.g. aneurysm)
461
First line Mx for non-functioning adenomas?
transsphenoidal surgery due to their compressive symptoms
462
Primary Mx for most pituitary adenomas?
- transsphenoidal surgery
463
If medical therpy is used for pituitary adenoma Mx, what would be used for prolactinomas? GH-secreting adenomas? ACTH secreting adenomas?
- P= dopamine agonists eg. cabergoline
- GH= somatostatin analogues eg. octreotide or GH-recept antag eg. pegvisomant
-ACTH= cortisol synthesis inh eg. ketoconaxole and neuromodulators eg. pasireotide
464
When is radiotherapy indicated for pituitary adenomas?
For residual or recurrent tumours post-surgery
465
Thyroid eye disease?
Affects 25-50% pts with Graves. Autoimmune response causes orbital inflam causing collagen and glycosaminoglycan deposition in muscles.
466
RFs for thyroid eye disease?
Smoking, radioiodine treatment
467
Thyroid eye disease CP
conjunctival oedema, optic disc swelling, inability to close eyelids- dry eyes- risk of exposure keratopathy.
468
Mx of thyroid eye disease?
smoking cessation, topical lubricants to prevent corneal inflamm caused by exposure, steroids, radiotherapy, surgery
469
Cx of thyroid eye?
Exposure keratopathy, optic neuropathy, strabismus and diplopia
470
Primary aim of investigating thyroid nodules?
To exclude thyroid cancer (5% of nodules)
471
Thyroid nodules Ix?
Ultrasonography
472
Benign and malignant causes of thyroid nodules?
B= mutlinodular goitre, thyroid adenoma, Hashimotos, cysts.
M= papillary carcinoma, lymphoma
473
Toxic multinodular goitre?
thyroid gland containing a number of autonomously functioning thyroid nodules resulting in hyperthyroidism. Nuclear scintigraphy reveals patchy uptake.
474
Mx for toxic multinodular goitre?
Radioiodine therapy
475
Phaeochromocytoma?
tumour of the adrenal glands that secretes unregulated and excessive amounts of catecholamines (adrenaline).
About 10% are familial and may be associated with MEN type II, neurofibromatosis and von Hippel-Lindau syndrome
476
Phaeochromocytoma basics?
bilateral in 10%
malignant in 10%
extra-adrenal in 10% (most common site = organ of Zuckerkandl, adjacent to the bifurcation of the aorta)
477
Phaeochromocytoma features?
typically episodic (relate to periods when tumour is secreting adrenaline)
HTN (may be sustained)
headaches
palpitations
sweating
anxiety
478
Phaeochromocytoma Ix?
24 hr urinary collection of metanephrines
479
Phaeochromocytoma Mx?
Surgery is the definitive management.
The patient must first however be stabilized with medical management:
- alpha-blocker (e.g. phenoxybenzamine), given before a
beta-blocker (e.g. propranolol)
480
Phaeochromocytoma pathophysiology?
Adrenaline is produced by the chromaffin cells in the medulla (middle part) of the adrenal glands. Adrenaline is a catecholamine hormone that stimulates the sympathetic nervous system and is responsible for the “fight or flight” response.
A phaeochromocytoma is a tumour of the chromaffin cells that secretes unregulated and excessive amounts of adrenaline. In patients with a phaeochromocytoma, the adrenaline tends to be secreted in bursts, giving intermittent symptoms.
481
How is cortisol produced?
CRH produced by hypothalamus -> stimulates anterior pituitary to produce ACTH -> acts on adrenals -> cortisol produced by zona fasiculata layer in adrenal cortex
482
When is cortisol usually secreted?
throughout the day, peaks at 6am
- also in response to stress= fight or flight; hypoglycaemia; infections; caffeine, sleep deprivation
483
Main function of cortisol
steroid hormone (glucocorticoid) that helps regulate metabolic and immune pathways
484
How does cortisol help regulate the immune response eg. as it is released in response to infection?
promotes overall anti inflamm state by inhibiting: prostaglandins, leukotrienes and interleukin-2 production by WBCs (P & L products of inflam)
485
How does cortisol help with hypoglycaemia?
Promotes gluconeogenesis in liver= this is production of new glucose. Also increases insulin resistance in tissues so insulin less effective at moving glucose into cells so blood glucose increases.
Also stimulates proteolysis: breakdown of proteins into amino acids in muscles, these are substrates for gluconeogenesis
486
How does cortisol play a role in maintaining BP?
up-regulates alpha1 adrenergic receptors in blood vessels which causes vasoconstriction
487
How does cortisol decrease bone formation?
inhibits new production by osteoblasts, suppresses Ca absorption and decreases production of type I collagen
488
Functions of cortisol?
1) anti-inflam
2) stimulates metabolic pathways (lipolysis, gluconeogenesis and proteolysis) to maintain normal glucose concs
3) maintains BP
4) improves brain performance
5) decreases bone formation
489
What stimulates ACTH secretion?
- throughout day, peaks at 6am
- stress= infection, hypoglycaemia, low BP
(as acts on adrenals to produce glucocorticoids eg. cortisol)
490
Glucocorticocoid example?
- cortisol
491
ACTH functions?
- act on adrenals to secrete glucocorticoids eg. cortisol
- acts on melanocortin receptor 1 (responsible for skin pigmentation) so if ACTH XS get bronzing of skin
492
Diuresis?
XS urine production
493
2 actions of ADH?
water retention and vasocontriction
- these increase BP
494
XS sweating eg. on hot day leads to what?
dehydration and so increased blood osmolarity (same amount of solutes but less water)
495
What detect changes in osmolarity?
osmoreceptors in supraoptic nuclei of hypothalamus
496
What is the thirst response that happens when blood osmolarity increases (eg. dehydrated)?
1) osmoreceptors in supraoptic nuclei of hypothalamus detect the change
2) water moves out of aquaporin 4 channels in cells into the blood by osmosis
3) osmolarity past 290-300 causes neurons to fire action potentials that signal hypothalamus to trigger the thirst response
497
Role of ADH when blood osmolarity increases?
1) ADH released by posterior pituitary
2) act on vasopressin receptor 2 in kidneys (distal convoluted tubule and collecting ducts of the nephrons)
3) when ADH binds to receptors, a G protein inside the cell gets activated that then signals adenylyl cyclase to convert ATP to cAMP
4) increased cAMP signals cells to produce more aquaporin 2 (water channels)= allows water to travel out lumen of tubule, into cells lining nephron then into blood
5) dilutes blood (like drinking water)
498
How does ADH respond to low blood volume?
1) low blood volume = low BP
2) low BP detected by baroreceptors near carotid artery in neck and arch of aorta
3) signals ADH secretion
4) causes vasocontriction and water retention
2) also the renin angiotensin system
499
Role of renin when there is low blood volume?
2) baroreceptors in afferent artery of kidneys (juxtaglomerular cells)
3) cause kidneys to secrete enzyme renin
3) renin converts angiotensinogen in the liver to angiotensin I
4) angiotensin converting enzyme (ACE) in the lungs then concerts angiotensin I to angiotensin II
5) angiotensin II stimulates more ADH production in hypothalamus
6) ADH causes vasocontriction and water retention
500
How does ADH (vasopressin) maintain blood pressure and plasma osmolarity?
1) acts on vasopressin receptor 2 in distal convoluted tubule and collecting ducts of the nephron to increase water reabsorption through aquaporins= decreases blood osmolarity
2) acts on vasopressin receptor 2 in walls of blood vessels to cause vasoconstriction and increase in peripheral resistance= increase BP
(baroreceptors and release of renin)
501
What happens when blood pressure decreases and renin-angiotensin-aldosterone system is activated?
1) baroreceptors in juxtaglomerular cells in afferent arteriole (next to glomerulus in kidney) detect this
2) causes enzyme renin to be released by kidney
3) renin converts angiotensinogen (in liver) to angiotensin I
4) angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II
5) angiotensin II causes vasocontriction of blood vessels, an increase in ADH (P.Pituitary) and the production of aldosterone in the kidneys
6) ADH increases thirst and water reabsoption as well as vasoconstriction and increasing peripheral resistance
7) late response of RAAS: aldosterone helps regulate sodium balance by acting on cells that line distal tubules and collecting ducts
8) aldosterone gets into these cells and bind its receptor which increases the expression (levels) of sodium/potassium ion pump
9) this pump pushes sodium
and water into blood and potassium into cells
502
Electrolyte disturbance in pts with intense activation of RAAS?
hypokalaemia (sodium potassium pump activated by aldosterone pulls K into cells and pushes Na and H20 into blood)
503
Decrease in BP can be detected by what?
baroreceptors of the carotid sinus or aortic arch; juxtaglomerular cells; or macula densa cells sensing less Na and Cl flowing through the tubules
causes kidneys to secrete renin
504
Role of aldosterone?
sodium and water retention
and increased elimination of K
505
What when baroreceptors in juxtaglomerular cells are stretched (due to increase BP) vs when collapsed (from low BP)?
stretched= inhibit renin release
collapsed= stimulate renin release
506
How do mechanoreceptors (baroreceptors) in carotid sinus and aortic arch measure BP and help regulate BP?
stretched= sympathetic NS will be downregulated
collapsed= SNS will be activated
sympathetic nerves stimulate b1 adrenergic receptors on JG cells to stimulate renin
507
How to macula densa cells help regulate BP?
they are chemoreceptors that sense when GFR increases or decreases based on the quantity of Na and Cl ions flowing through tubule
1) BP rises= renal blood flow and so GFR increases
2) so means more fluid reaching macula densa
3) if decreased fluid then the MD cells send signal to JG cells in afferent arteriole (signal is prostaglandins) to stimulate renin
so NSAIDs can block prostaglandin signal and impair response of kidney to reduce BP
508
Role of angiotensin II?
1) vasoconstriction of blood vessels
2) production of aldosterone in kindey
3) release of ADH by posterior pituitary
4) thirst response= signals tp hypothalamus to increase thirst
509
How does aldosterone increase BP?
increases water & sodium retention, and increases the elimination of potassium
- acts on cells lining the distal tubules and collecting ducts, causes increased expression (levels) of Na/K ion pump which pushes sodium and water into blood and pulls K into cells
510
Summary of how ADH responds to low BP?
1) water retention= acts on vasopressin receptor 2 in distal convoluted tubule and collecting ducts of nephron to increase water reabsorption through aquaporins= decreasing blood osmolality
2) vasocontriction and increase in peripheral resistance
511
Thirst response?
angiotensin II signals to hypothalamus or
osmoreceptors detect change (increase osmolality) in supraoptic nuclei of hypothalamus, causes neurons to fire action potentials that signal to hypothalamus to increase thirst
512
3 things that detect low BP?
1) baroreceptors in juxtaglomerular cells that stimulate renin release
2) baroreceptors in carotid sinus & aortic arch that will collapse= stimulates sympathetic NS= sympathetic nerves stimulate b1 adrenergic receptors on JG cells to stimulate renin production
3) macula densa cells (chemoreceptors) sense decreased GFR (& so decreased fluid) so send signal to JG cells to stimulate renin release (signal is prostaglandins)
513
Why can NSAIDs impair kidneys response to low BP?
block prostaglandin signals from macula densa cells (detect low BP) to JG cells that stimulate release of renin
514
What hormones does the hypothalamus secrete?
Act on anterior pituitary:
- Stimulatory hypothalamic hormones= TRH, CRH, GnRH, GHRH
- Inhibitory hormones= GHIH (somatostatin) and prolactin inhibiting factor (dopamine)
Act on posterior pituitary:
- ADH (vasopressin) and oxytocin
515
Anterior vs posterior pituitary?
Anterior= hypothalamic hormones act on and stimulates anterior pituitary to produce and release its own hormones
Posterior= stores hormones in Herring bodies (ADH and oxytocin produced by hypothalamus)
516
What in the hypothalamus produces ADH and oxytocin that is stored in posterior pituitary?
paraventricular and supraoptic nuclei of hypothalamus
517
TRH?
Thyrotropin releasing hormone
518
Thyrotropin releasing hormone?
hypothalamus produces TRH -> acts on anterior pituitary and stimulates it to make thryoid stimulating hormone (TSH) -> acts on thyroid -> increase in thyroid hormone production
519
CRH?
corticotropin releasing hormone
520
Corticotropin releasing hormone?
hypothalamus produces CRH -> acts on AP -> ACTH -> acts on adrenals -> cortisol
521
Growth hormone releasing hormone?
hypothalamus makes GHRH -> AP -> GH production -> acts on long bones and other tissues
522
Increased levels of plasma cortisol inhibit...
ACTH production in anterior pituitary through negative feedback to decrease cortisol production
523
GHRH?
growth hormone releasing hormone
524
GnRH?
gonadotropin releasing hormone
525
Gonadotropin releasing hormone?
hypothalamus makes GnRH
-> AP -> gonadotrophins (FSH and LH) -> acts on gonads:
1) regulate production and maturation of gametes (testes= sperm, ovaries= oocytes)
2) stimulates production of sex hormones= testosterone, oestrogen, progesterone
- females= oestrogen spikes before ovulation, makes AP more sensitive to GnRH so surge of FSH and LH to stimulate ovulation (+ve feedback)
526
GHIH?
growth hormone inhibiting hormone (somatostatin)
527
Growth hormone inhibiting hormone (somatostatin)?
GHIH also made in GI tract (and hypothalamus), tells AP to produce less GH
528
Prolactin inhibiting factor (dopamine)?
prolactin inhibiting factor (dopamine) -> AP -> inhibits prolactin production
during breastfeeding= suckling signals to hypothalamus -> haults production of PI factor so prolactin is produced
529
ADH (vasopressin) stands for?
anti diuretic hormone
530
ADH (vasopressin) use?
released by posterior pituitary when blood osmolarity increased or blood volume decreased -> vasoconstriction of blood vessels and water retention (& Na) from urine -> decreases osmolarity and increases BP
531
Oxytocin?
released by posterior pituitary during motherhood / small amounts following social interaction (hug, orgasm)
- dilates cervix, stimulates uterine contractions during childbirth, causes breast muscles to contract to eject milk
532
Pineal gland?
behind hypothalamus and pituitary
pinealocytes make and release melatonin (mostly at night)
533
Melatonin?
regulates circadian rhythm (tells us when to sleep and wake)
534
3 things that make up the thyroid gland that secrete hormones?
1) follicular cells= T3 and T4 (most of T4 converted to T3 as T3 increases basal metabolism rate)
2) parafollicular cells= calcitonin
3) parathyroid gland (4 total, 2 each lobe)= parathyroid hormone
535
Role of calcitonin and PTH (secreted in thyroid)?
involved in calcium, bone and phosphate metabolism
levels regulated by calcium blood levels
536
Structure of adrenal glands and what hormones they secrete?
Medulla (centre)= adrenaline and noradrenaline
Cortex (outer) 3 layers:
1) zona Glomerulosa (outer)= mineralcorticoids eg. aldosterone
2) zona Fasiculata= glucocorticoids eg. cortisol
3) zona Reticularis (inner)= sex hormone precursors
537
Main hormones secreted in adrenals?
1) aldosterone secreted when BP low or increased blood K -> water and Na retention and increased elimination of K
2) cortisol secreted during fight or flight alongside adrenaline and noradrenaline by medulla
538
2 parts of the pancreas?
Exocrine part= secretes digestive enzymes into duodenum
Endocrine part= Beta cells (secrete insulin) and Alpha cells (glucagon)
539
Pancreas response to hyperglycaemia?
B cells secrete insulin -> binds to receptors on all cells in body so they take in glucose for energy -> decreases blood glucose after eating
540
Pancreas response to hypoglycaemia?
Alpha cells secrete glucagon -> binds to receptors on liver cells -> releases enzymes to break down glycogen (bodys glucose store) in liver -> released as glucose into blood to increase blood glucose
541
