Endocrinology Flashcards

1
Q

what are the blood results for Addison’s?

A

Hyponatraemia
Hyperkalamiae
hypoglycaemia
metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

how do we manage type 2 DM?

A

first start lifestyle changes
if HbA1C rises to 48 on lifestyle advice, add Metformin

if HbA1C rises add a second medication from the following:

  • Gliptin (DDP4 inhibitor)
  • sulfonylurea
  • SGLT-2 inhbitor
  • pioglitazone

if, despite the 2nd med, HbA1C rises to/or remains above 58mmol/mol - add a 3rd med

triple therapy with any of the following combinations:
- metformin + sulfonylurea + pioglitazone
- metformin + sulfonylurea + SGLT-2 inhibitor
- metformin + sulfonylurea + gliptin
- metformin + pioglitazone + SGLT-2 inhibitor
or consider insulin therapy

finally, if triple therapy not working
a GLP-1 analogue can be tried in combination with metformin and a sulfonylurea if BMI>35 with obesity related problems or <35 but cant take insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

how do we manage idiopathic adrenal hyperplasia?

A

aldosterone antagonists e.g. spironolactone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are the targets in DKA treatment?

A

reduce ketones by 0.5 mmol/L/h
reduce glucose by 3 mmol/L/h
increase bicarb by 3 mmol/L/h
maintain potassium between 4-5.5mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are side effects of pioglitazone?

A

weight gain, osteoporosis, swelling of legs/ankles, risk of liver disease, anaemia risk, fluid retention

contraindicated in previous bladder cancer patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what usually precipitates HHS (hyperglycaemic, hyperosmolar state)?

A

infection, MI, stroke or other acute illness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

how do DDP4 inhibitors/gliptins work?

give names of drugs

A

DDP-4 enzymes are involved in deactivating incretins (GLP-1). by inhibiting them - we raise the levels of GLP-1 which bind to Beta cells and increase insulin production and secretion.

e.g. sitagliptin, vildagliptin, linagliptin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how does the BD (biphasic) insulin regime work?

A

patient takes 2 premixed insulin doses - via disposable pens
good for a regular lifestyle
twice‑daily insulin detemir is the regime of choice.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the causes behind primary hyperparathyroidism?

A
usually - adenoma (80% cases)
multifocal disease (10-15%)
carcinoma (<1%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are side effects of sulfonylureas?

A

weight gain, hypoglycaemia, upset stomach, skin rash/itching

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are 3 features of Hashimoto’s thyroiditis?

A

hypothyroidism
goitre
anti-TPO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

which thyroid cancer secretes calcitonin?

A

medullary cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

when do we treat subclinical hypothyroidism?

A

if TSH is btwn 4-10
for <65s with symptoms - treat with a trial of levothyroxine and continue if shows improvement
if asymptomatic or older - watch and wait, repeat TFTS in 6 months

if TSH is >10
for <70s - treat with levothyroxine
watch and wait for older patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

at what HbA1C level do we add a second drug to metformin for T2DM patients?

A

58

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is involved in the HPA axis?

A

Hypothalamus secretes corticotropin releasing factor (CRF)
CRF stimulates the anterior pituitary to secrete ACTH
ACTH stimulate the adrenal cortex to secrete cortisol and androgens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

which is the insulin regime of choice for adults?

A

multiple daily basal-bolus injections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

which drugs can cause hypercalcaemia?

A

thiazide diuretics

calcium containing antacids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is an important complication of fluid resuscitation in young DKA patients?

A

cerebral oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

whats the most common cause of Addison’s worldwide?

A

Tb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

tell me about ultra fast acting insulin

A

examples = novorapid, humalog

used to inject before a meal or just after. helps to match insulin to what is actually eaten

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

when do we consider transferring a DKA patient to ICU?

A
if there are signs of severe DKA:
pH < 7 
bicarb < 5 
blood ketones > 7 
GCS < 12 
K+ < 3.5 
oxygen sats <92% 
low BP or pulse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

how do you classify BMI into normal/overweight/obese?

A
normal= 18.5 - 25 
overweight =25-30
obese 1 =30-35
obese 2 =35-40
obese 3 =>40
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is the MoA of carbimazole?

A

it blocks thyroid perioxidase from iodinating the tyrosine residues on the thyroglublin - this reduces the production of thyroid hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are side effects of Gliptins?

A

usually well tolerated

can cause hypoglycaemia, hives, fluid retention, UTI, headaches, facial swelling nasopharyngitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
how do we manage pregnancy in diabetic patients?
in advance, have a target of 48mmol/mol! take folic acid 5mg OD during pregnancy, have a blood glucose control assessment every 1-2 weeks throughout pregnancy
26
what are the TFT levels in subclinical hypothyroidism?
elevated TSH with normal T4
27
what is the single most useful test in determining the cause of hypocalcemia?
parathyroid hormone
28
which are the 2 most common thyroid cancers?
papillary (70%) | follicular (20%)
29
what are symptoms of hyperglycaemia?
``` polyuria polydypsia lethargy genital thrush weight loss visual blurring ```
30
what are the clinical features of Paget's disease?
only 5% are symptomatic bone pain - lumbar spine, femoral, pelvis skull bossing, leg bowing raised ALP, normal phosphate and calcium skull xray - thickened vault
31
what is the pathophysiology of secondary hyperparathyroidism?
parathyroid hyperplasia occurs in response to low calcium, almost always in a setting of chronic renal failure
32
what are the findings in hyperaldosteronism?
``` raised BP raised/normal sodium low potassium raised bicarbonate (alkalosis) raised aldosterone low renin ```
33
which steroid has high GC activity and low MC activity?
dexamethasone and betmethasone | important if we need high anti inflammatory action and low fluid retention e.g. in cranial tumours
34
why electrolyte deficiency is responsible for sustained hypocalcaemia despite calcium replacement therapy?
magnesium | magnesium is needed for PTH secretion and its action on target tissues
35
how much potassium should we give to DKA patients?
if potassium is >5.5 give nil if potassium is 3.5-5.5 give 40mmol/L infusion if < 3.5 - seek help
36
what are the symptoms of hyperaldosteronism?
can be asymptomatic signs of hypokalaemia= cramps, weakness, paraesthesia High BP and headaches
37
which hormones are reduced in the stress response?
insulin oestrogen testosterone
38
what are side effects of treatment with levothyroxine?
hyperthyroidism reduced bone mineral density worse angina atrial fibrillation
39
what is Waterhouse - Friderichsen syndrome?
adrenal failure due to haemorrhage into the adrenal gland, commonly caused by severe infection severe form of meningococcal sepsis usually pre-terminal patients present with sepsis, coagulopathy, extremities cyanosed, comatosed
40
whats the most important advice to give a patient being started on carbimazole?
if they get any signs of infection they should seek urgent medical review a rare side effect = agranulocytosis
41
what's sick euthyroid syndrome?
its caused by systemic disease total and free T4 and T3 are minimally low TSH is normal or slightly low
42
how do we investigate hyperaldosteronism?
``` 1st line = renin:aldosterone ratio High serum aldosterone low serum renin adrenal vein sampling high resolution CT scan ```
43
how do we treat phaeochromocytoma?
surgery is definitive treatment | but we first stabilise the patient with alpha blockers (phenoxybenzamine) and then beta blockers (propanolol)
44
what is kussmauls breathing?
heavy respiration - expiring CO2 to try and compensate for metablic acidosis
45
what are the features of LADA?
these patients, although they have autoimmune disease, like type 1 DM, are picked up later in life. their diabetes progresses a lot slower - and may not need insulin in the earlier stages LADA can often be misdiagnosed at T2 DM but patients are usually younger and less obese diagnosis may be aided by GAD autoantibody testing or other autoimmune disease
46
what is Cushing's disease?
pituitary tumour secreting ACTH causing adrenal hyperplasia
47
what ABG results are associated with Cushings?
hypokalaemic metabolic alkalosis
48
give an example of a fluid replacement regime in a DKA patient?
1st hour: 0.9% saline - 1L | 2nd hour: 0.9% saline + potassium chloride
49
what glucose ranges are diagnostic for diabetes?
fasting glucose >7 | HbA1C >48
50
where is ADH secreted from and what does it do?
ADH is released for the posterior pituitary in response to thirst. ADH causes more aquaporin channels to be inserted into collecting duct membranes in the kidneys. this increases water retention
51
what are the causes for hyperkalaemia?
``` AKI drugs - K sparing diuretics, ACE-I, ARBs, spironolactone metabolic acidosis massive blood transfusion addisons rhabdomyolosis ```
52
what percentage of pre-diabetic patients progress to type 2/year?
5-10%
53
how do we treat an adrenal tumour?
for adenoma - adrenalectomy | for carcinoma - radiotherapy and adrenolytic drugs
54
which mutation is associated with most cases of MODY?
mutation in the HNF1- alpha gene | known as MODY 3
55
how do we treat hypoparathyroidism?
with alfacalcidol | which is an analogue of vitamin D
56
what glucose ranges show prediabetes?
42-47 HbA1C | fasting glucose: between 6-7
57
what do the osteoporosis guidelines recommend regarding a postmenopausal woman who has had a fracture?
give her bisphosphonate and calcium supplements
58
when do you NOT have to inform the DVLA about taking insulin?
if on temporary insulin for < 3 months | or because of gestational diabetes and wont be continuing the insulin for more than 3 months postpartum
59
what does thyrotoxicosis alongside a singular hot nodule (on scintography) indicate?
toxic adenoma | this occurs when a single nodule grows on the thyroid gland - producing excess hormones and causing thyrotoxicosis
60
what are the features of type 2 DM?
associated with lack of exercise, obesity, alcohol and calorie excess more common in asians, men and elderly because of excess adipose tissue, there is a relative insulin insufficiency - not enough to go around
61
which anti diabetic drug increases insulin sensitivity?
pioglitazone
62
how does diabetes causes damage to the eyes? (2)
1) endothelial changes causes capillary leakage - causing intraretinal oedema which then forms hard exudates. in the macular area this can result in loss of central vision 2) capillary occlusion can cause retinal ischaemia. in the macular area this can cause visual loss. the ischaemia then causes new retinal vessels forming. the new vessels can cause - haemorrhage, fibrosis, etc all leading to total blindness
63
how is Addison's managed?
steroid replacement therapy | hydrocortisone (in 2 or 3 doses per day) and fludrocortisone
64
what are the features of MEN 1?
3 Ps (parathyroid, pituitary and pancreas) and adrenal and thyroid
65
whats the most serious potential complication of AKI?
hyperkalaemia
66
how do we investigate phaeochromocytoma?
24 hour urinary collection of metanephrines VMA in urine is usually elevated and serum metanephrines are elevated
67
what is MEN?
multiple endocrine neoplasia | autosomal dominant disorder
68
where is prolactin produced?
anterior pituitary gland
69
what is the pathophysiology of primary hyperaldosteronism?
excess aldosterone leads to Sodium reabsorption, H2O retention and K+ excretion. this leads to raised blood pressure, hypernatraemia, hypokalaemia, and alkalosis
70
what are side effects to long term steroid use?
endocrine - impaired glucose regulation, hyperlipidaemia, excess hair growth, increased appetite/weight gain bones - osteoporosis, osteopaenia, avascular necrosis of the femoral head, immunosuppression GI - peptic ulceration and pancreatitis psychiatric - mania, psychosis, insomnia, depression cushings syndrome - moon face, buffalohump, stria eyes -glaucoma, cataracts intracranial hypertension suppression of growth in children
71
how do you identify a benign incidental adrenal adenoma?
usually picked up on CT accidentally | the ademona has a rich lipid core with well circumscribed nodules
72
what are signs of thyrotoxicosis?
tachycardia, maybe irregular pulse, moist warm skin, fine tremors, lid lag/retraction, goitre, thin hair, thyroid nodules/bruit.
73
how do we manage a prediabetic patient?
encourage to make lifestyle changes - exercise and change diet (more fibre less fat) consider 500mg OD metformin test HbA1C regularly - annually
74
how do we define diabetes?
hyperglycaemia levels sufficient to cause microvascular complications
75
how often should a T1 DM patient check his blood glucose/day?
at least 4 times a day - before meals and before bed
76
what are symptoms of hyponatramea?
dizzy, nausea, headache, coma if severe, signs of dehydration or fluid overload
77
tell me about premixed insulins
e.g. novamix 30 | 30% SA and 70% LA
78
which glucose ranges show normal glycaemic control?
HbA1C < 42 | fasting glucose < 7
79
what diabetic medication should we consider as first line for a patient with end-renal failure?
Gliclazide | Metformin is contraindicated (can't be used in any patient with eGFR < 30)
80
is a Type 2 diabetic patient, on insulin, allowed to drive a HGV?
yes, but he must meet very strict criteria set out by the DVLA, relating to hypoglycaemia
81
what are the 2 main causes for hypercalcaemia?
primary hyperparathyroidism malignancy these 2 causes account for 90% of cases
82
what is MODY?
a group of genetic diseases affecting the production of insulin maturity onset diabetes of the young usually in those < 25 years with a strong family history typically autosomal dominant number of genes identified patients usually very sensitive to sulfonylureas
83
what are the 5 types of thyroid cancer?
``` papillary follicular medullary anaplastic lymphoma ```
84
how is HHS diagnosed?
signs of dehydration osmolarity: >320mosmol/kg hyperglycaemic: >30mmol/L with pH>7.3 and no ketonaemia < 3mmol/L
85
what are the complications of pagets disease?
``` deafness - CN trapping bone sarcoma skull thickening fractures high output cardiac failure ```
86
how would a patient present in phase 1 of subacute thyroiditis ?
tender goitre hyperthyroidism raised ESR globally decreased uptake on iodine scan (Technetium scan)
87
tell me about long acting/basal insulin?
human insulin analogues e. g. glargine - used at bedtime, to give a steady insulin baseline all night. good for those who struggle with nocturnal hypoglycaemia e. g. detemir
88
what investigation should we do in a patient who's drowsy, vomiting, dehydrated, abdo pain, polyuria, polydipsia?
CHECK BLOOD GLUCOSE
89
what does thyroxine interact with??
iron iron reduces the absorption of thyroxine take the drugs 2 hours apart
90
what is the mechanism of action of sitagliptin?
it is a dipeptidyl peptidase 4 inhibitor (DPP-4) | this prevents the breakdown of GLP-1, therefor increasing its levels and so increasing insulin
91
what rate of insulin should u prescribe for ketoacidotic patients?
0.1 unit/kg/hour
92
what medication can we use pre-op to decrease cortisol secretion?
metyrapone, ketocanozole, flucanazole
93
how do patients with hypercalcaemia present?
non specific symptoms | nausea, polydipsia, polyuria, weakness, confusion, constipation
94
what antibodies are associated with Graves disease?
TSH receptor stimulating antibodies | anti-thyroid peroxidase antibodies
95
how do we prevent diabetic retinopathy?
primary prevention - BP and glucose control secondary - regular assessment immediate anti VEGF treatment in diabetic macular oedema - to prevent new vessels forming e.g. ranibizumb, aflibercept 3) salvage therapy - vitrectomy
96
whats the best investigation to differentiate between type 1 and type 2 diabetes?
C peptide this will be low in type 1 (because the pancreas is not producing enough insulin precursor which breaks down to give insulin and C-peptide) and normal or high in type 2
97
how does the OD insulin regime work?
once a day, taking a dose of LA insulin good started for T2 patients switching across to insulin typical dose is around 1 unit/BMI unit/24 hours can retain metformin etc if need for tighter control
98
how do we screen for acromegaly?
by testing serum Insulin-like Growth factor -1 IGF-1, which represents 24 hour GH levels
99
what are the features of type 1 DM?
usually presents in adolescents/young adults at risk of ketoacidosis and weight loss antibody destruction of pancreatic, insulin-producing beta cells (anti bodies include Glutamic acid decarboxylase (GAD) antibodies and islet cell antibodies (ICA) associated with other autoimmune disease treated with insulin
100
what is acromegaly?
excessive GH | in 95% of cases this is secondary to a pituitary adenoma
101
what is Paget's disease?
a disease of excessive turnover of the bone - increased osteoclast and osteoblast activity
102
how do we monitor for subclinical recurrence of medullary thyroid carcinoma?
calcitonin levels
103
what is congenital adrenal hyperplasia?
a group of autosomal recessive diseases in response to low cortisol, the pituitary gland produces excess ACTH which leads to increased production of androgens leading to large build, manly hair, early menarche
104
what is the synacthen test?
ACTH stimulation test | ACTH is injected and the cortisol response is measured.
105
how do we diagnose DKA?
1) acidosis - pH <7.3 or Bicarb <15 2) hyperglycaemia - glucose>11 (or13.8) or known Diabetes 3) ketosis - ketonaemia >3 or ++ on dipstick
106
who's more likely to develop diabetes: a patient with impaired fasting glycaemia or impaired glucose tolerance?
those with impaired glucose intolerance are more likely
107
how do we manage HHS?
rehydrate slowly - with 0.9% saline, over 48 hours replace K+ once urine starts to flow use insulin if glucose not falling by 5mmol/L/kg/H OR if there is ketonaemia keep blood glucose at least 10-15mmol/L to avoid cerebral oedema
108
what is LADA?
latent autoimmune diabetes of adult
109
what features are specific to graves disease?
eye signs - exophalmus, ophalmoplegia pretibial myxoedema thyroid acropachy
110
how do we treat hyperaldosteronism?
if its due to Conn's = laprascopic adrenalectomy | if its due to hyperplasia = treat medically with spironolactone or amiloride
111
what are side effects of SGLT-2 inhibitors?
UTI, weight loss, change in urination, genital yeast infections, upper resp tract infections
112
what causes primary hyperaldosteronism ?
idopathic adrenal hyperplasia (70% cases) adrenal adenoma - Conn's syndrome adrenal carcinoma - rare
113
how do we treat an addisonian crisis?
100mg iv/im hydrocortisone saline with dextrose (if hypoglycaemic) continue steroids 6 hourly until stable
114
what dietary advice do we offer diabetic T2 patients?
include in your diet plenty of high fibre and low glycaemic index foods. oily fish, low fat diary products reduce intake of high energy carbs, saturated fats, trans-fatty acids weight loss of 5-10% fat in obese patients
115
what are ACTH independent causes of Cushings?
iatrogenic - steroid use adrenal nodular hyperplasia adrenal adenoma/cancer
116
how do we manage hypercalcaemia?
first - IV saline! -patient will be dehydrated then once hydrated can give bisphosphonates e.g. IV pamidronate calcitonin can be given to patients who are resistant to bisphosphonates
117
what are the causes of primary hyperparathyroidism ?
80% cases = solitary adenoma 10-15% cases = multifocal disease 1% carcinoma
118
how do we treat Addison's disease?
replace steroids 15-25 mg hydrocortisone/day 50-200mcg fludrocortisone
119
what population is Graves disease typically seen in?
females, aged 30-50
120
what does ACTH stand for?
adrenocorticotropic hormone
121
when should orlistat be stopped?
if the patient has lost more than 5% weight in 12 month s
122
what are the symptoms of hypoparathyroidism?
the symptoms are mostly secondary to hypocalcaemia ``` muscle spasms, twitching, cramping chvostek's sign Trousseau's sign perioral parasthesia ECG long QT ```
123
how do we diagnose asymptomatic diabetes?
random glucose >11 or fasting glucose > 7 must be demonstrated on 2 separate occasions
124
what is diabetes insipidus?
it can either be cranial (not enought ADH produces) or nephrogenic (kidney insensitive to ADH) patients produce large quantities of dilute urine - polyuria and drink a lot to compensate - polydypsia people can become dehydrated if they are unable to drink
125
which TFT results show poor thyroxine compliance?
High TSH and normal T4 this is because TSH takes longer to normalise, so the patient could have had low thyroxine before coming to the doctor, but taken her medication before her blood test so her T4 is normal but her TSH hasn't corrected yet Raised T4 with raised TSH also points towards poor compliance. the patient has taken extra tables prior to blood test causing the raised T4 but TSH hasnt had time to be suppressed (TSH levels take days to weeks to change)
126
if a patient with Addison's disease is ill, should there be changes made to their medication?
yes, hydrocortisone should be doubled (because the body would usually increase its production during illness- stress response) fludrocortisone can be kept the same
127
what are the causes for galactorrhoea ?
``` 6 Ps pregnancy physiological primary hypothyroidism prolactinoma polycystic ovarian syndrome phenothiazines, domperidone, metaclopramide ```
128
what is phaeochromocytoma?
a rare catecholamine secreting tumour
129
in regards to insulin, how do we manage a patient with DKA?
start him on a fixed IV insulin of 0.1 units/kg/hour
130
how does SIADH present?
solitary hyponatraemia, water retention
131
what are common precipitating factors for DKA?
missed insulin dose infection myocardial infarction
132
what are the features of DKA?
dehydration, polyuria, polydipsia abdominal pain , vomiting , drowsiness kussmauls respiration - deep hyperventilation sweet smelling breath - acetone
133
which blood cells might increase with corticosteroid use?
neutrophils | CS are thought to cause neutrophilia via 3 mechanisms.
134
what type of drug is gliclazide?
sulfonylurea
135
what are the signs of thyroid eye disease? (as seen in almost 50% cases of Graves disease)
``` exophthalmus - protruding eye appearance proptosis - eye protudes beyond orbit othalmoplegia conjuntival oedema papillodeama corneal ulceration ```
136
what are contraindications for radioiodine treatment?
pregnancy - should be avoided for 4-6 months after as well | thyroid eye disease is a relative CI- can be made worse
137
how are thyroid hormones synthesised?
thyroid follicular cells produce thyroglobulin (Tg) iodine is transported and trapped in the colloid Thyroid perioxidase (TPO) on the luminal surface of TFCs iodinates the tyrosine residues on the Tg (this is known as organification) the iodinated Tg are endocytosed by the follicular cells and are hydrolised there to produce thyroid hormones. (mostly T4) they are then secreted into the blood - bound to globulins. in peripheral tissues, T4 is deionised to produce T3
138
where is iodine deficiency most common?
africa, asia, himalayas
139
when should you refer a patient to the diabetic foot clinic?
if they have any foot problems besides for simple calluses
140
what are symptoms of a prolactinoma in female?
infertility oligomenorrhoea galactorea
141
what risk factor modification medication should diabetic patients be on?
ACE-I if BP>140/80 statins if 10-year CVD risk is >10% anti-platelets
142
what are the levels in secondary hyperparathyroidism?
Raises PTH low or normal Calcium High Phosphate Low Vit D
143
how does the QDS insulin regime work?
this regimen is useful for those with a flexible/changing lifestyle. patient takes ultra fast acting insulin before meals/exercise and then a LA analogue at night
144
how do we treat symptomatic prolactinoma?
with dopamine agonists which inhibit the release of prolactin from the pituitary gland e.g. Bromocriptine if the DAs are not tolerated, surgery is the next option. trans-sphenoidal hypophysectomy
145
why does potassium fall in DKA treatment?
insulin makes the cells take up potassium
146
what are the symptoms of Addison's disease??
lethargy, weakness, anorexia, nausea, weight loss, vomiting, salt craving hyperpigmentation, vitilgo, loss of pubic hair in females hypotension crisis = collapse, shock, pyrexia
147
what are the features of acromegaly?
coarse facial features, spade like hands, bigger feat oily skin, excessive sweating prognathism, large tongue, interdental spaces symptoms of intracranial mass- headaches, bitemporal hemianopia raised prolactin in 1/3 of cases - galactorrhoe
148
what are the features of addisonian crisis?
hyponatraemia hyperkalaemia hypoglycaemia hypovolaemia
149
what is an important worry in HHS and how do we prevent it?
``` occlusive events (DIC, chorea, focal CNS signs, leg ischaemia/rhabdomyolosis) give prophylactic LMWH ```
150
how is osteoporosis linked to graves disease?
excess T3 causes increased osteoclast activity leading to excess bone resorption - causing osteoporosis
151
in patients admitted with hypercalcaemia, when is IV bisphosphonate indicated?
when calicum is over 3
152
how do we treat painful diabetic neuropathy?
the same way as we treat any neuropathic pain 1) first line treatment = amitryptaline, pregablin, gabapentin, duloxetine 2) if the medication doesnt work, try another of the 4 drugs tramadol can be used as rescue therapy topical capsaicin can be used for topical pain
153
how do we confirm a diagnosis of acromegaly ?
with an OGTT normally, hyperglycaemia leads to suppression of GH - but this doesnt happen in acromegaly we perform the OGTT with series of GH tests after
154
what is ketogenesis?
its an alternative metabolic pathway - to provide energy to cells. its inefficient and produces acetone without insulin, glucose can't enter the cells, so the body thinks it is 'starving' - and ketogenesis kicks in, as a last resort
155
what are the symptoms of hypothyroidism?
lethargy, tired, weak, cramps, cold intolerance, weight gain, cramps, hoarse voice, constipation, menhorragea, myalgia
156
what is a grand mal seizure?
its a tonic clonic seizure | loss of consciousness with strong muscle contractions
157
what is primary hyperaldosteronism ?
excessive production of aldosterone, independent of the RAA axis
158
what are the 'sick-day rules' for diabetic patients?
try drink 3L/24hour maintain normal insulin regime if dehydrated- possible stop metoformin check ketones regularly - every 3-4 hours check glucose levels more frequently - every 4 hours if ketones are raised take a corrective insulin dose (usually normal dose divided by 6 - not more than 15 units) have sugary drinks if struggling to eat
159
how does pioglitazone work?
helps to decrease insulin resistance (aka increase insulin sensitivity) in peripheral tissues and liver decreases gluconeogenesis and levels of glucose/glycated Hb in bloodstream
160
what are hormone levels in primary hyperparathyroidism?
raised PTH, raised calcium, low phosphate
161
what are important side effects of SGLT2 inhibitors
genital infections | diabetic ketoacidosis
162
what is Addison's disease?
primary adrenocortical insufficiency | destruction of the adrenal cortex leading to corticosteroid and aldosterone deficiency
163
what are complications of DKA and its treatment?
``` hypoglycaemia hypo/hyperkalaemia - can cause arrhythmias cerebral oedema thromboembolism AKI gastric stasis respiratory destress ```
164
what % of thyrotoxicosis cases are due to graves?
60-70%
165
what is considered hypoglycaemic?
glucose < 4
166
what causes secondary hypothyroidism? how is it detected?
TFT results of low TSH and low T4 suggests pituitary insufficiency pituitary disease will cause secondary hypothyroidism - rare MRI pituitary should be ordered to investigate further
167
how does phaeochromocytoma present?
``` typically episodes of: hypertension headaches sweating anxiety palpitations ```
168
how do we treat pagets disease?
bisphosphonates | oral Risedronate or IV zoledronate
169
what is the first line insulin regime offered to adults with T1 DM?
basel-bolus regime with twice daily detemir
170
why does diabetic foot disease occur?
1) neuropathy - loss of protective sensation, charcots arthropathy 2) peripheral arterial disease -macro/microvascular ischaemia
171
what is hashimoto's thyroiditis?
an autoimmune thyroid disease, associated with hypothyroidism 10 times more common in women features include anti-TPO antibodies and anti - Tg antibodies non-tender goitre
172
tell me about short acting insulin
isophane it has a variable peak at 4-12 hours cheap - favoured by NICE
173
what does OGGT stand for?
oral glucose tolerance test
174
what are causes of thyrotoxicosis?
``` graves disease toxic nodular goitre acute phase of subacute thyroiditis acute phase of hashimoto's htyroiditis acute phase of post-partum thyroiditis amiodarone therapy ```
175
what is the cushing's triad?
3 clinical signs resulting from raised ICP 1) irregular breathing 2) bradycardia 3) systolic hypertension
176
how do we manage thyrotoxicosis?
carbimazole - either via titration or block and replace method titration: start on carbimazole 40 mg and titrate down until euthyroid state is reached. continued for 12-18 months. titration results in less side effects than block and replace. block and replace: give carbimazole 40mg and then thyroxine is added when the patient reaches euthyroid. treatment usually lasts 6-9 months. radio-iodine and surgery are also options
177
which hormones are produced by the anterior pituitary?
``` TSH GH LH/FSH Prolactin Endorphins ACTH ```
178
what are daily blood glucose targets for T1 DM patients?
5-7 on waking | 4-7 before meals
179
what are the symptoms of HHS?
signs of dehydration, polydypsia, weakness, leg cramps, altered mental states, trouble sleeping
180
how do sulfonylureas work? | give names of drugs
they increase Beta cell activity and insulin release (by binding to, and closing potassium channels - they lead to raised calcium levels and fusion of insulin granules with cell membrane) e.g. gliclazide, glipizide, glibenclamide
181
how do we narrow down the cause of hyponatraemia?
1) we first assess if the patient is in a state of fluid overload or dehydrated 2) if the patient is dehydrated - we check the urinary sodium. if the urinary sodium is high (>20mmol/L)- we know the sodium is being lossed in the urine. causes can include: addisons, renal failure, diuretics 3) if the urinary sodium is low, the sodium is being lossed elsewhere - perhapes in burns/vomit/diarrhoea etc 4) if the patient is not dehydrated, we check to see if they are oedematous, if they aren't - we look at urine osmolarity. if it is high,causes = SIADH if it is low = water overload 5) if the patient is oedematous - causes can include = CF, renal failure, cirrhosis, nephrotic syndrome
182
how do WHO define diabetes?
fasting glucose > 7 levels 2H post glucose load >11.1 HbA1C > 48
183
what is Trousseau's sign?
carpal spasm of the hand when BP cuff is inflated to higher than systolic pressure it is a sign of hypocalcaemia
184
whats the best investigation for suspected Addison's disease?
ACTH stimulation test if not available- can do a 9am cortisol test. if >500 it rules out Addison's. if <100 it's an abnormal result. between 100-500, an ACTH stimulation test is indicated
185
how do we manage primary hyperparathyroidism and nephrolithiasis (kidney stones)??
exploration and parathyroidectomy
186
how do we assess treatment response in hypothyroidism patients?
TSH levels | aim of treatment is to normalise the TSH levels
187
how is paget's disease defined?
isolated raise of ALP with x-ray changes
188
what are the features of MEN 2a?
Medullary thyroid carcinoma and 2Ps - Pheochromocytoma and parathyroid
189
what is Nelsons syndrome?
rapid enlargement of pituitary corticothroph adenoma (ACTH secreting tumour). this occurs post bilateral adrenalectomy (an old popular treatment for cushings disease/syndrome)- so there is no negative feedback by cortisol on ACTH production - leading to proliferation of any pre-existing pituitary adenoma. the growth leads to physical compression affects such as headaches and visual distrubances. the high levels of ACTH can cause MSH (melanocyte stimulating hormone) production and hyperpigmentation
190
how do we manage thyroid cancer?
total thyroidectomy radioiodine treatment to remove residual cells thyroglobulin monitoring to detect early recurrent disease
191
what are the signs/symptoms of diabetic autonomic neuropathy?
impaired pupil adaptation, dry skin, tachycardia, orthostatic hypotension, silent myocardial ischaemia, exercise intolerance gastroperisis, constipation/diarrhoea, oesophageal dysmobility, genitourinary dysfunction - erectile dysfunction, retrograde ejaculation, female sexual dysfunction
192
what are signs of hypothyroidism?
bradycardia, thin hair and skin, drowsy, yawning, cold hands, decreased temp, fluid overload, goitre
193
what is the best way to treat MODY 3?
sulfonylureas (glicazide) are optimal treatment for HNF1-a mutations
194
what causes secondary hyperaldosteronism?
increased renin due to decreased kidney perfusion. this can result from renal artery stenosis, diuretics, CCF, hepatic failure
195
which thyroid carcinoma is associated with genetic inheritance?
medullary carcinoma it can be inherited in an autosomal dominant pattern may also be alongside a pheocromocytoma
196
what is the most common cause of thyrotoxicosis?
Graves disease
197
what is the most common cause of secondary adrenal insufficiency?
iatrogenic - steroids lead to suppression of the HPA axis. when steroids are withdrawn, addison's is apparent
198
what are other names for subacute thyroiditis?
De Quervains thyroiditis | subacute granulomatous thyroiditis
199
how do we manage hypoglycaemia?
if patient conscious and cooperative -give quick acting 20g carb if uncooperative - squeeze glucagel into mouth if unconscious - IV/IM glucose 1mg once glucose >4, give long acting carb e.g. toast
200
what are glucose targets for T2 Diabetic patients?
on lifestyle advice or lifestyle advice + metformin - the target is 48mmol/mol with a second medication added, target is 53mmol/mol
201
what are side effects of metformin?
upset stomach, sickness with alcohol, kidney complications, dizziness, tiredness, metal taste
202
what are levels in secondary hyperparathyroidism?
raised PTH, low calcium, raised phosphate, low Vit D
203
how do patients with primary hyperparathyroidism present?
``` bones renal stones abdominal groans psychic moans - depression hypertension polyuria polydypsia ```
204
how do we manage DKA?
1) fluid resuscitation. isotonic saline used at first 2) insulin -IV. (0.1 unit/kg/hour) 3) once insulin is < 15 mmol/mol then 5% dextrose infusion should be started (to prevent hypoglycaemia) 4) continue normal LA insulin regime 5) treat hyperkalaemia (calcium and then potassium)
205
what are causes of primary hypothyroidism?
hashimoto's thyroiditis - most common, autoimmune disease subacute thyroitis hyperthyroid treatment - ATD, radioiodine, surgery iodine deficiency (leading cause worldwide) drugs - amiodarone, lithium riedel thyroiditis - inflammatory condition of the thyroid, replacing the tissue with fibrosed tissue
206
what are the phases for subacute thyroiditis?
usually post viral infection phase 1 - hyperthyroidism, painful goitre, raised ESR (3-6 weeks) phase 2 - euthyroid (1-3 weeks) phase 3 - hypothyroidism (weeks to months) phase 4 - thyroid structure and function returns to normal
207
which drugs can cause SIADH?
``` sulfonylureas SSRIs, triclyclics carbamazapine vincristine cyclophosphamide ```
208
how often do we check HbA1C in diabetic patients?
3-6 monthly until stable | and then every 6 months
209
what percentage of diabetic patients have type 2?
90%
210
what are names for pre-diabetes syndromes?
impaired glucose tolerance (IGT) | impaired fasting glucose (IFG)
211
what levels are raised in congenital adrenal hyperplasia?
raised 21 deoxycortisol raised 17 deoxyprogesterone raised urinary adrenocorticosteroid metabolites
212
why are Free T3/4 measurements more reliable than Total T4/3?
total T4 / T3 measurements rely on TBG (thyroid binding globulin). TBG goes up in pregnancy, hepatitis and oestrogen therapy TBG goes down in malnutrition, nephrotic syndrome, CLD, acromegaly
213
how do patients with diabetic foot disease present?
neuropathy - loss of sensation ischaemia - absent foot pulses, reduced ankle brachial index pressure, claudication complications - ulceration, gangrene, charcots arthropathy, osteomyelitis, calluses, cellulitis
214
what are the symptoms of thyrotoxicosis?
diarrhoea, palpitations, sweat, overactive, irritable, weight loss, increased appetite, oligomenorrhea, labile emotions, heat intolerance, tremors,
215
a patient presents with hypercalcaemia, recurrent peptic ulcerations and milky nipple discharge, what do you suspect?
MEN type 1 | causing parathyroid, pancreas and pituitary tumours (3Ps)
216
which group of people is papillary cancer most commonly observed?
young females
217
what are the layers of the adrenal gland and what hormones do they produce?
there is the cortex and the medulla the cortex is divided into 3 layers: 1) zona glomerulosa - produces mineralcorticoids - aldosterone 2) zona fasciculata - produces glucocorticoids - cortisol etc 3) zona reticularis - produces androgens the medulla produces catecholamines e.g. E and NE
218
what can cause ectopic ACTH production?
small cell lund cancer | carcinoid tumour
219
how do SGLT-2 inhibitors work? | give names of drugs
they inhibit the sodium-glucose cotransporter in the in the kidney. mainly expressed in the PCT. prevents glucose being absorbed by the kideys - so passed out in urine e.g.' -gliflozin' dapagliflozin, empagliflozin
220
how do we diagnose diabetes?
1) symptoms AND random glucose>11.1/fasting glucose>7 2) asymptomatic AND random glucose>11.1/fasting glucose>7 on 2 separate occasions 3) HbA1C >48 mmol/mol
221
what causes Addison's disease?
80% of cases are autoimmune in the UK world wide- the main cause is Tb other causes = haemorrhage, congenital, lymphoma, opportunistic infections in HIV
222
how do we diagnose diabetes insipidus?
water restriction test
223
how do hypoglycaemic patients present?
sweaty, increased pulse, seizures, odd behaviour (maybe aggression), decreased mental state
224
how do we stratify diabetic foot according to risk ?
low risk - no risk factors present moderate risk - 1 risk factor present e.g. neuropathy/ischaemia/deformity high risk - previous amputation/ulceration or on renal replacement therapy or >1 risk factor present e.g. loss of sensation/ signs of PAD
225
how do we initially treat hyperkalaemia?
calcium gluconate or calcium chloride - stabilises the myocardial membrane potential
226
what are the features of MEN 2b?
Medullary thyroid carcinoma and 1P -pheochromocytoma | and marfinoid body habitus and neuromas
227
what should initial starting dose of levothyroxine be?
50-100mcg OD | this should be lower in elderly patients and those with ischaemic heart disease
228
what is Chvostek's sign?
tapping over the parotid (CN7) causes facial muscles to twitch a sign of hypocalcaemia
229
when should we add metformin for T1 DM?
if BMI >25
230
how do we confirm a diagnosis of cushings syndrome?
using the dexamethasone suppression test 1) we give 1 mg dexamethasone at 10 pm at night and then take serum cortisol levels at 9 am the next day. if the cortisol level is not suppressed by negative feedback from this extra steroid - we can confirm excess steroids and cushings syndrome 2) we then do the high dose (8 mg) dexamethasone suppression test to differentiate between cushings disease (pituitary adenoma) or another source. if the cortisol is suppressed - we know it is cushings disease. if it is NOT suppressed, the raised cortisol will either be due to 1) an ectopic ACTH source or 2) an adrenal cushings which is independent of ACTH to differentiate between these 2 options, we measure the ACTH. if the ACTH is low then it is an adrenal cushings (independent of ACTH), and if it is high, the cortisol level is due to an ectopic ACTH producing tumour
231
what is the best way to decrease the risk of thyroid eye disease?
stop smoking
232
what types of insulins are there?
ultra-fast acting , short acting, long acting and mixed
233
should we alter thyroxine doses in pregnant women?
yes, by 25-50mcg - because of the increased demand
234
what are the criteria for prescription of Orlistat?
BMI >28 with risk factors or BMI >30 with continued weight loss e.g. 5% at 3 months use for <1 year
235
what are causes for an addisonian crisis?
surgery/sepsis exacerbating a chronic deficiency adrenal haemorrhage steroid withdrawal
236
is hyperpigmentation seen in primary or secondary adrenal insufficiency ?
primary this is because lower cortisol production from adrenal glands leads to positive feedback of ACTH production. more ACTH leads to more MSH, causing pigmentation
237
how do we manage gastroperesis?
``` with prokinetic agents including erythromycin methoclopramide domperidone ```
238
what are the levels in primary hyperparathyroidism ?
High PTH High Calcium Low phosphate
239
how is SIADH treated?
fluid restriction
240
when do we feel thirst?
if plasma osmolarity increases - either due to decreased water or increased electrolytes (mainly sodium)
241
what are considerations when prescribing pioglitazone?
its contraindicated with history of bladder cancer (it can increase the risk of bladder cancer), heart failure (because can cause fluid retention), in obese patients may increase weight
242
when is bariatric surgery indicated?
BMI > 40 or >35 with significant disease tried all other medical/lifestyle treatment fit and well for surgery committed to long term follow up
243
whilst awaiting brain imaging, how do we treat a patient with suspected brain metastases?
high dose dexamethasone | will reduce cerebral oedema
244
what is Sheehan's syndrome?
secondary hypothyroidism due to pituitary infarction post-partum (due to big haemorrhage during labour) patients will also probably be low in other pituitary hormones - prolactin, ACTH, gonadotropins
245
what are the symptoms of hypercalcaemia?
``` bones - pain stones - renal groans - abdo, nausea, vomiting thrones - polyuria pshyc overtones - confusion, cognitive impairment ```
246
what age does Cushings disease most commonly occur?
30-50s
247
what does a combination of hypothyroidism and a goitre point towards?
hashimoto's thyroiditis
248
how do you investigate subacute thyroiditis?
globally low uptake on iodine - 131 scan
249
which anti-diabetic medication causes weight gain?
sulfonylurea
250
which anti-diabetic drug can cause gastroperesis?
GLP-1 agonists e.g. | liraglutide
251
what is suspected in a young patient with asymptomatic hyperglycaemia?
MODY | MODY3 being the most common - mutation in HNF1alpha gene
252
what are MODY3 patients more at risk of?
hepatocellular carcinoma
253
what is a rare complication of steroid therapy?
steroid psychosis