Endocrinology Flashcards
(176 cards)
1
Q
target blood pressure for t2dm
A
140/90
if pt has retinopathy, cerebrovascular disease or microalbuminuria = 130/80
2
Q
DPP4 inhibitor patient weight
A
do not cause weight gain
3
Q
types of diabetic retinopathy
A
non-proliferative diabetic retinopathy (NPDR), proliferative retinopathy (PDR) and maculopathy.
4
Q
features of mild NPDR
A
1 or more microaneurysm
5
Q
management for all patients with diabetic retinopathy
A
optimise glycaemic control, blood pressure and hyperlipidemia
regular review by ophthalmology
6
Q
management of Non-proliferative retinopathy
A
regular observation
if severe/very severe consider panretinal laser photocoagulation
7
Q
what are cotton wool spots
A
reprisent areas of retinal infarction
8
Q
features of Moderate NPDR
A
microaneurysms
blot haemorrhages
hard exudates
cotton wool spots, venous beading/looping and (less severe) intraretinal microvascular abnormalities (IRMA)
9
Q
pathophysiology of diabetic retinopathy
A
Hyperglycaemia –> increased retinal blood flow and abnormal metabolism in the retinal vessel walls –> damages endothelial cells and pericytes
Endothelial dysfunction –> increased vascular permeability –> characteristic exudates seen on fundoscopy.
Pericyte dysfunction predisposes to the formation of microaneurysms.
Neovasculization is caused by the production of growth factors in response to retinal ischaemia
10
Q
What is the function of insulin?
A
to drive glucose into cells when not needed
to inhibit ketone production when not needed
11
Q
what are ketones need for?
A
to supply energy to brain during periods of hypoglycaema
12
Q
what occurs during hypoglycaemia / starvation at hormone level
A
LOW insulin
HIGH glucagon / cortisol etc
this causes GLYCOGEN to be taken out of cells > converted back to GLUCOSE
KETONE production
13
Q
What will fasting and OGTT tests be in T1DM
A
Fasting blood glucose >7
OGTT >11.1
14
Q
what is normal, prediabetes and diabetes HbA1c
A
Normal: <42
Prediabetes: 42 - 48
Diabetes: >48
15
Q
what are classical sx of diabetes and why?
A
TRIAD; fatigue, polyuria,polydipsia
as glucose is an osmotic diuretic, so it pulls out water
16
Q
features of diabetic neuropathy
A
- distral symmetrical sensory neuropathy (tingling, numbness, loss of vibration, proprioception and pain), loss of ankle jerk
- Gastroparesis (food passess slower) = abdominal pain, nausea, vomting
- Neuropathic pain
- toes clawing, loss of plantar arch, neuropathic ulcers, joint deformity (charchot foot)
17
Q
What is diabetic foot secondary to?
A
- diabetic neuropathy: glove and stocking sensory loss
- reduced oxygen: Peripheral arterial disease -> absent foot pulses, intermittent claudication
18
Q
how do you check for diabetic foot neuropathy
A
10g monofilament test, done at least annually
19
Q
how do you check for diabetic NEPHROPATHY
A
Yearly ACR (albumin : creatinine ratio)
20
Q
what is the first sign of diabetic nephropathy=
A
microalbuminuria: ACR> 2.5
21
Q
what is the effect of ACEi on AKI, CKD and diabetic nephropathy
A
TOXIC in AKI
PROTECTIVE in CKD and diabetic nephropathy
22
Q
when must you stop an ACEi
A
when there is a drop in GFR >20%
23
Q
what is ACEi’s initial effect of GFR
A
initial drop due to dilating of the efferent arteriole
24
Q
How often do you monitor cap glucose in T1 diabetes
A
4x a day in adults, 5x a day in children
25
How can you manage T1DM
- BASAL BOLUS REGIMEN (rapid insulin with meal, long acting insulin BD)
OR
- Twice daily BIPHASIC INSULIN (which is a mix of long and short acting)
26
When is basal bolus regimen most appropriatw
when patients are bale to count carbs and ensure that sufficient insulin is taken per meal
27
Give examples of short acting insulin
Actrapid
| Novorapid
28
Give exaplines of long acting insulin
lantus
| levemir
29
give example of mixed biphasic insulin
Humulim M3
30
What HbA1c do you start metforminn for? WHen do you escalate to dual therapy?
Start METFORMIN if HbA1c >48 . dual therapy if >58
| DUAL THERAPY if HbA1c >58, aim for <53
31
conservative management for T2DM
patient education
diet (high fibre, low GI carb, low salt and saturated fats)
regular exercise + weight loss
smoking cessation
target BP 140/90 unless has disease 130/80
manage high cholesterol
32
montoring for T2DM
* Monitor HbA1c 6mthly
* Annual screen for
o Retinopathy
o Diabetic food problems
o Nephropathy
o Cardiovascular risk factors
o Injection site problems if on insulin
33
How do you manage T2DM first line
1. Metformin max 2g/day
34
What is MoA of metformin
increases insulin sensitivity
| decreases hepatic gluconeogenesis
35
side effects of metformin
appetite suppression, diarrhoea, lactic acidosis
36
what do you do if metformin is causing diarrhoea
change to modified release
37
when is metformin contraindicated
if eGFR <30 (renal failure), cardiac failure and hepatic failure --> lactic acidosis
| if tissue hypoxia e.g. MI, surgery
38
When do you upscale to adding another drug to metformin
when HbA1c >58
39
how do sulphonylureas work
↑Secretion of insulin from pancreatic beta cells
40
side effects of sulphonylurea
weight gain, HYPOGLYCAEMIA (esp in renal impairment)
41
give examples of sulphonylurea
glibenclamide, gliclazide, tobutamide
| gliclazide
42
what is method of action of gliptins (DPP4 inhibitor)
Inhibit breakdown of GLP-1 increases insulin secretion reduces glucagon secretion
43
give example of gliptin
SITAGLIPTIN
44
when is a sulphonylurea contraindicated
when patient is already fat
| or if ketoacidotis
45
give example of SGLT 2 inhibitore
Dapagliflozin, Empaglifloxin
46
slgt2 inhibitor mechanism of action
They lower the renal threshold for glucose increased urinary glucose excretion
47
HbA1c targets
48
dual therapy for T2DM
* Metformin + gliptin (DPP4 inhibitor)
* Metformin + sulfonylurea
* Metformin + pioglitazone (Thiazolidinediones)
* Metformin + SGLT2 inhibitor
49
What can you give if triple therapy for T2DM?
Metformin + sulphonylurea + other
50
what can you give for T2DM after triple therapy?
Metformin + sulphonylurea + GLP1 analogue
51
Why does HHS cause high glucose but not high ketones
because there is insufficient insulin to drive glucose into cells
but still enough insulin to inhibit ketone production
52
List causes of hyperthyroidism
high uptake:
1. **Graves disease**
2. **Toxic multinodular goitre**
3. **Toxic adenoma**
low uptake:
1. **Subacute De Quervains thyroiditis (Viral thyroiditis**)
2. **Post partum thyroiditis**
53
De Quervain's thyroiditis (viral thyroiditis) sx/s
* severe viral illness (**fever, myalgia, malaise**) --> attacks the thyroid gland
* Period of **hyperthyroidism** -> **hypothyroidism**, then **euthyroid** (as stored thyroxine released, then eventually becomes exhausted)
* Enlarged, tender, firm thyroid -> **Painful dysphagia**
54
What occurs in Graves disease
Anti TSH R antibodies (igG)
| This leads to increased thyroid function and thyroid growth
55
Signs of Graves’ disease
1. **Diffuse smoothly enlarged GOITRE**
2. **proximal myopathy**
3. **lid lag** (eyelid lags behind eye’s descent as patient watches your finger descend)
4. brisk reflexes
*signs specific to grave's disease*
1. EYE signs:**Exophthalmos**: protruding eyes, due to THSr Ab on eye muscles and Ophthalmoplegia: **diplopia**
2. **Pretibial myxoedema**: non-pitting oedematous swellings above lateral malleoli
3. **Thyroid acropachy** (digital **clubbing** + soft tissue swelling of hands/feet + periosteal new bone formation)
56
thyroid storm signs
sudden onset severe hyperthyroidism:
o **Fever** > 38.5
o **Tachycardia** (+/- AF)
o **hypertension** or Volume depletion —> **hypotension**
o **Confusion and agitation**
o **Nausea and vomiting**
o **Abdominal pain**
o **Heart failure** – listen to heart and lung bases
o **Jaundice and abnormal LFTs**
o **Thyroid bruit**
57
Management of Acute thyroid storm
o **ABCDE** : **Fluid resuscitation**, Oxygen if needed
o **High dose** **propylthiouracil** or **carbimazole**
o **Dexamethasone** (block conversion of T4 to T3)
o**IV propranolol IMMEDIATELY**
o **Analgesia**
o **Lugol’s Iodine**: Delayed until 4 hours after antithyroid therapy (inhibits the release of stored thyroid hormone)
58
How do you investigate suspected graves
* TFTs - **low TSH + high T3/T4** (High T3/T4 ratio suggests Graves > thyroidits)
* Autoantibodies: Anti-TPO (75%), Anti-thyroglobulin, **TSH-receptor Ab** - (very sensitive and specific)
* Imaging: **Thyroid ultrasound**: highly vascular, enlarged thyroid, **Technetium-99 uptake scan**: **diffuse HIGH uptake**
59
How do you manage Graves
1. Symptom relief: Beta blocker **PROPANOLOL**
2. Anti thyroid drug: **Carbimazole** (high dose and titrate down), **Propylthiouracil**
3. **Radioactive iodine** (risk of permament hypothyroidism)
4. Surgery: **thyroidectomy** is last resort
60
causes of hypothyroidism
Autoimmune:
1. **Primary atrophic hypothyroid** (commonest cause in the UK)
2. **Hashimotos thyroiditis**
Other:
1. **Iodine deficiency** (most common worldwide)
2. **Post thyroidectomy/radioiodine**
3. **Drug induced** - antirthyroid drugs, lithium, amiodarone
61
What is Hashmoto's
AI cause of HYPOTHYROIDsm
due to anti-TPO Ab (also anti thyroglobulin)
62
How do you manage hypothyroidism
**Levothyroxine** - aim for normal TSH (0.5 – 2.5 mU/L) - *lower dose if cardiac diseas*e (inc myocardial contractilit --> risk of ischaemia)
* rule out **underlying adrenal insufficiency** before starting thyroid hormone replacement --> can precipitate an **Addisonian crisis**
63
what will extreme hypothyroidism cause and how does it present
it causes **MYXOEDEMA COMA**
presents as **hypothermia**, **Hypoventilation**, **Hyponatraemia, Hyporeflexia, Bradycardia, Heart failure, Seizures, Confusion, Coma**
64
How do you manage myxoedema coma
IV T4/T3 – **liothyronine** (IV T3) is given as faster onset of action
**IV hydrocortisone** (until adrenal insufficiency ruled out)
**IV fluids**
**Oxygen rewarming**
**treat underlying cause** (e.g infection)
65
Where and what hormones are produced by the adrenal
ZG: Mineralocorticoids (ALDOSTERONE)
ZF: Glucocorticoids (Cortisol)
ZR: Androgens
Medulla: Adrenaline, NA
66
What triggers production of cortisol
the HPA axis (CRH > ACTH >cortisol)
67
what is aldosterone produced in respnse to
* dec renal perfusion pressure, dec Na or inc renin SNS activity or decreased --> renin released
* also inceased K+
68
what can aldosterone bond to
Mineralocorticoid R
69
What does aldosterone induce
SODIUM REABSORTPION > WATER REABSORPTION
| POTASSIUM EXCRETION
70
what is the fucntion of glucocorticoids
to regularte glucose balance
71
What are causes of adrenal insufficiency
PRIMARY (high ACTH) : Addison's (AI) or TB, causing adrenal gland destruction
SECNODARY (low ACTH) : Pituitary adenoma / sheehan's
TERTIARY: brain tumour
72
How does adrenal insufficiency prsent
fatigue, anorxia, WL
GI sx: nausea, vomiting, abdo pain, diarrhoea, constipation
**hyperpigmentation (raised ACTH) **
**low BP (insufficient fluid and salt retention)**
vitiligo
loss of body hair
73
How do you investigate adrenal insufficiency
1. 9AM cortisol --> if LOW (< 100 nmol/L) : suspect
2. short synacthen test (ACTH stimulation test) --> Serum cortisol < 550 nmol/L at 30 mins is suspect
3. adrenal antibodies
4. MRI pituitary gland
| 2. adminisrter short synachten test
74
How do you manage adrenal insufficiency
Hydrocortisone (GC) and fludrocortisone (MC)
if secondary --> only hydrocortisone needed
advice: wear a medic-alert bracelet, have a steroid warning card
| o Hydrocortisone dosage needs to be increased during times of acute illn
75
what is addisonian crisis
* acute adrenal insufficiency, often precipitated by stress (infection, surgery)
* hypoglycaemia + hypotension + hypothermia
76
HJow do you manage acute addisonian crisis
* Rapid IV fluid rehydration
* IV 200 mg hydrocortisone bolus --> Followed by 100 mg 6 hourly hydrocortisone until BP is stable
* Assess glucose if hypoglycaemia, consider dextrose
* Treat precipitating cause (e.g. antibiotics for infection)
* Monitor BP, glucose, fluid status, Na, K
77
complications of adrenal insufficiency
o HYPERKALAEMIA
o Death during Addisonian crisis
o Overreplacement of glucocorticoids:
78
What are the two sizes of a pituitary adenoma
microadenoma <1cm
| macroadenoma > 1cm
79
Whayt is the commonest type of pituitary adenoma
PROLACTINNOMA
| causes hyperprolactinoma
80
presentation of prolactinoma in women
* High prolactin ->**galactorrhoea**
* Low GnRH -> low LH and FSH:
**Amenorrhoea/oligomenorrhoea
Infertility
Hirsuitism
Reduced libido
Weakness (osteoporosis)
Dry vagina**
81
presentation of prolactinoma in men
* Low GnRH ->low LH and FSH
**Reduced libido
Impotence
Infertility
Reduced beard growth
Erectile dysfunction**
* High prolactin -> galactorrhoea, gynaecomastia (rare)
82
how do macroprolactinomas cause symptoms
as the prolactinoma grows, the pituitary compresses the optic chiasm --> bitemporal hemianopia (loss of peripheral vision), headache, diolopia, ophthalmoplegia
83
ix for prolactinoma
* **exclude pregnancy**
* bloods: **TFT** (hypothyroidism as prolactinoma suppresses TRH), **serum prolactin level**
* **visual field testing**
* **MRI PITUITARY** (DIAGNOSTIC)
84
prolactinoma mx
1st line = Dopamine agonists: **Bromocriptine, Cabergoline**
2nd line = Surgery: **trans-sphenoidal excision **
| transnasal hypophysectomy
85
what is cushings syndrome caused by
*EXCESS CORTISOL*
**Exogenous GC therapy or Endogenous**:
- **ACTH dependent (80%)**: excess ACTH from a **pituitary adenoma (Cushings disease**) or **ectopic** ACTH production from **SCLC**, **carcinoid tumour**
- **ACTH independent**: *suppressed ACTH* = steroids (most common cause), **benign adrenal adenoma, adrenal carcinoma**)
86
what is CUSHINGS DISEASE
Excess ACTH from pituitary gland, usually due to pituitary tumour
87
Signs of cushings syndrome
o **Moon face**
o Facial plethora: **red cheeks**
o Interscapular fat pad – **buffalo neck hump**
o **Supraclavicular fat distribution**
o **Proximal myopathy**
o **Pink/purple striae** on abdomen/breast/thighs
o **Kyphosis** (due to vertebral fracture)
o **Hypertension**
o **Ankle oedema** (due to salt and water retention from the mineralocorticoid effect of excess cortisol)
o **Pigmentation** in ACTH dependent cases
o **Osteoporosis**
o **increased susceptibility to infection**
88
Sx of cushings syndrome
Symptoms (lemon on a stick):
o **Increasing weight**
o **Fatigue**
o **Muscle weakness**
o **Myalgia**
o **Thin skin**
o **Easy bruising**
o **Poor wound healing**
o **Fractures**
o Gonadal dysfunction – **Hirsuitism, irregular menses, erectile dysfunction, gynaecomastia (men )**
o **Acne**
o **Frontal balding**
o **Recurrent Achilles tendon rupture
o Depression or psychosis**
89
Ix for Cushings syndrome
1. **Overnight dexamethasone suppression test**
2. **24hr urinary free cortisol**
3. **Low dose dexamethasone suppression test**
4. **Inferior petrosal sinus sampling** (identifies pituitary disease)
90
What does LDDST show
after dexamethason:
- if cortisol is low > normal suppression
- if cortisol is still high > confirmed Cushings synsrome, perfome Inferior Petrosal Sinus Sampling (IPSS)
91
medical management of cushings
**SHORT TERM USE ONLY** - Used pre-operatively or if unfit for surgery
o **Metyrapone**
o **Ketoconazole**
92
How do you manage pituitary adenoma
surgery: trans-sphenoidal adenoma resection
93
How do you manage adrenal mass causing Cushing syndrome
Adrenalectomy + steroid replacement
94
What is Conns syndrome
**Primary hyperaldosteronism**
**Excess ALDOSTERONE ONLY** > excess salt and water reabbsorption (**hypertension**), excess potassium excretion (**hypokalaemia**) --> renin release is suppressed
95
causes of Conns syndrome
adrenal adenoma
96
How does Conns present
Symptoms of Hypokalaemia: **Muscle weakness, Cramps, Polyuria and polydipsia (Hypok can induce nephrogenic DI), Paraesthesia, Tetany**
Signs:
* **HTN refractory to tx**
* hypertensive retinopathy
* oedema
97
How do you ix Conns
* **U&Es**: LOW K+, NORMAL/HIGH NA+ (Serum Na usually normal because Na reabsorption is matched by water reabsorption)
* **Plasma aldosterone / renin ratio** (high)
* ECG: **arrhythmias**
* Confirmatory Tests: **Salt Loading** (2 week high sodium diet), CT/MRI
98
What is Plasma aldosterone / renin ratio like in RAS
normal
| becuase it is the high renin that raises aldosterone
99
How do you manaage CONNS
- spironolactone / eplerenone
- surgery (laparoscopic adrenalectomy
| avoid surgery in elderly
100
How does PTH control calcum
HIGH PTC causes:
- **increased Ca release from bone**
- renal: **increases Ca2+ reabsorption and PO4 excretion,** **increases calcitriol formation via 1a-hydroxylase** --> **increased Ca absorption in GI**
101
what must you check first in hypercalcaemia
PTH serum
102
what is primary Hyperparathyroidism and what causes it
**increased secretion of PTH by parathyroid gland** unrelated to the plasma calcium concentration
* **inappropriately Normal/high PTH** -> **high calcium and low phosphate**
Causes:
- PT adenoma (80%)
- PT hyperplasia (20%)
- PT carcinoma (<0.5%)
103
what does low PTH in hypercalacemia tell you
Low PTH: hypercalcaemia of malignancy
- bone mets
- PTH producing Squamous cell carcinoma of lunng
- myeloma
104
Symptoms of hypercalcaemia (Ca >2.6)
**Stones** - *renal stones, polyuria, polydipsia*
**Bones**- *pain, osteopaenia and osteoporosis -> fractures*
**Abdo groans** - *abdo pain, N+V, peptic ulcer, constipation, pancreatitis*
**Psychic moans** - depression, lethargy
105
investigations for hyperparathyroidism
- **Exclude drug** causes of hypercalcemia: l**ithium, thiazide diuretics**
- U&Es (**PTH, Ca, PO4**)
- **albumin**
- **bone-speciic ALP**
- **vitamin D**
- **ABG** (Primary --> Hyperchloraemic acidosis ~ Due to PTH inhibition of renal reabsorption of bicarbonate)
- **Renal ultrasound**= can visualise renal calculi
- **DXA scan** for osteoporosis
106
How do you treat hypercalcaemi
**IV fluids 0.9% saline** IL over 1 hr
moniter calcium and vitamin D intake
treat cause:
- cancer: **parathyroidectomy**, **bisphosphonates**
- CKD: **Phosphate restriction + phosphate binder, Calcium supplementation**
- VIt d deficiency: **alfacalcidol**
107
what is secondary hyperparathyroidism and why does it occur
**increased secretion of PTH secondary to hypocalcaemia**
* **low/normal calcium and high phosphate** (kidneys not working) -> **high PTH**
caused by:
- **chronic renal failure** (most common)
- **vit D deficiency**
108
what is tertiary hyperparathyroidism and what causes it
**autonomous PTH secretion** (**despite high calcium**) following **chronic secondary hyperparathyroidism**
* high calcium, low phosphate, high PTH
* due to **end stage renal failure** or kidney transplant
109
how do you manage tertiary HPT
parathyroidectomy
110
what are blood results in pagets
raised ALP
everything lse normal
because this is a disease of excessive bone turnover
111
causees of B12 deficiency
Pernicious anaemia (AI)
Atrophic gastritis
Gastrectomy
Malnutrition
112
Signs of B12 deficiiency
Anaemia (lethargy, pallor, dyspnoea)
Neuro (peripheral neuropathy, weakness, ataxia, parasthesia)
Glossitis
Mild jaundicee
113
Ix for B12 deficiency
FBC (macrocytic anaemia, hypersecomented neutrophils)
b12 level
Anti IF Ab
Anti parital cell antibodies
114
management B12 deficiency
Severe: IM vitamin B12 (hydroxycobalamin, 3x weekly for 2 weeks, then three monthly injections)
Mild-moderate: PO / IM B12
115
How does subclinical hypothyroidims present on biochemistry?
High TSH but Normal T4/T3
116
what do you do with someone presenting with subclinical hypothyroidism
Repeat bloods in 6 weeks
117
What do you do if repeat TSH is elevated in subclin hypothyroidism?
TSH >10 : levothyroxine
TSH 5-10 + positive autoantibodies : repeat bloods in 1 year
TSH 5-10 and -ve antibodies : repeat bloods in 3-5 years
118
causes of HYPOCALCAEEMIA
1. PTH failure
2. Low vit D
3. Pancreatitis
4. Hypomagnesaemia
119
How do you investigate a thyroid neck lump that you are concerned about?
- **TFT**
- **thyroid autoaantibodies**
- **Thryoid USS +- fine needle aspirate**
- **thyroid uptake scan** (Multiple uptake hot nodules or Toxic adenoma~ solitary hot nodule)
120
classification of thyroid nodules
Single thyroid nodule: **solitary nodule**
* **Colloid and hyperplastic nodules**: benign lumps, can be solitary or part of multinodular goitre
* **Thyroid adenoma**: single benign lump
* **Thyroid cyst**: swelling containing fluid
* **Thyroid cancer**
Multiple thyroid nodules: **multinodular goitre**
* **Toxic MNG: Plummer’s disease**
121
signs and symptoms of thyroid nodules
Symptoms
* Mostly **ASYMPTOMATIC**
* **nodular goitre**
* A *single isolated nodule is more likely to be malignant*
* Sometimes cause **pain** and rarely compress the trachea or cause dysphagia
* Hyperthyroidism sx (**WL, inc appetite, diarrhoea, heat intolerance, anxiety, irritability, sweating, loss of libido oligomenorrhoea**)
Signs
* **Ask patient to drink some water** -> does the nodule move when swallowing?
* **Nodules and thyroglossal cysts both move on swallowing**, but only **cyst moves up on tongue protrusion**
* Check for regional **lymphadenopathy** (malignancy)
* Hyperthyroidism signs (**fine tremor, palmar erythema, tachycardia, thin hair, sweaty and warm palms, brisk reflexes, lid lag**)
* **Palpable solitary or multinodular goitre**
122
referral for thyroid nodule
● **Same day referral for stridor + thyroid mass**
● Two week referral for: **Unexplained hoarseness** / voice changes + **goitre**, **Rapidly enlarging painless thyroid mass** , Palpable **cervical lymphadenopathy**
Non-urgent referral :
* **Thyroid nodules + abnormal TFTs** → referral to **endocrinologist**
* **Sudden onset of pain within thyroid lump** (~ bleed into thyroid cyst)
123
treatment for toxic nodule
toxic = causing hyperthyroidism
● Beta-blockers, CCBs if intolerant of BB
● Anti-thyroid drugs: **Carbimazole / propylthiouracil**
● Radio-iodine (oral) → effects in 3-4 months
● Surgery: **subtotal / total thyroidectomy**
124
5 types of thyroid cancer
o Papillary (60%)
o Follicular (25%)
o Medullary (5%)
o Lymphoma (5%)
o Anaplastic (rare)
125
symptoms and signs of thyroid cancer
Symptoms
**o Slow-growing neck lump
o Hoarse voice
o Dyspnoea
o Dysphagia**
Signs
**o Palpable thyroid nodule or diffuse enlargement of thyroid
o Tracheal deviation
o Cervical lymphadenopathy
o Typically euthyroid**
126
how do ytou manage thyroid cancer
* total/hemi **thyroidectomy** + radioactive iodine ablation
* medullary and anaplastic = **thyroid replacement**
* papillary and follicular = **TSH suppression (levothyroxine)** as TSH sensitive
127
side effect of carbimazole
neutropoenia
agranulocytosis is a severe form of neutropenia
128
what is contraindication of giving radioiodine in graves disease
contraindicated in pregnancy or eye disease
129
what is complication of surgery to treat Graves
damage to recurrent laryngeal nerve > hoarseness
130
causes of HYPERNATRAEMIA
DEHYDRATON - LOSS OF WATER
- GI loss
- Sweat loss
- Renal loss (diabetes insipidus, diabetes mellitus)
INCREASE IN SODIUM
- iatrogenic
- high dietary intake
- Conn's
- RAS
131
How do you tell apart Conn's drom RAS
Using aldosterone : renal ratio
in CONNS, ARR is HIGH
In RAS, it is normal
132
how do you invesrigate HYPERnatraemiia
volume state - physical examination
- serum glucose (exclude diabetes)
- serum K+ (raised > Conn's. Low > nephrogenic DI)
- plasma and urine osmolarity (hyperaldosteronism: high plasma osmolarity)
- Water deprivation test (diabetes insipidus()
133
causes of cranial DI
* **Idiopathic** (50%)
* Trauma (e.g. **head injury, neurosurgery**)
* Tumours (e.g. **pituitary tumour, craniopharyngioma, metastases**)
134
causes of nephrogenic DI
**Idiopathic**
**Inherited**
Metabolic: **low potassium, high calcium**
**Chronic renal disease**
135
what test can you do for diabetes insipiitdu
**water deprivation test with despmopressin**
1. **fluid deprivation for 8 hours**- measure **plasma and urine osm every hour**. weigh patient hrly to monitor dehydration
2. stop test if if urine osmolality >600mOsmol/kg (normal)
3. **if < 600 --> give desmopressin**
4. **cranial DI = responds to desmopressin (urine osmolality rises > 50%**
5.**nephrogenic DI = DOESN'T responds to desmopressin (urine osmolality rises < 45%)**
136
treatment for diabetes insipidus
General: **Treat the CAUSE, Oral/IV fluids, Treat hyperNa**
Cranial DI
* Find cause: **MRI head**
* Give **desmopressin**
o If mild - **chlorpropamide or carbamazepine** -> potentiate the residual effects of any residual vasopressin
Nephrogenic DI
* **Fluids**
* **Sodium and/or protein restriction** helps polyuria
o **Thiazide diuretics** (bendroflumethiazide)
o **NSAIDs** lower urine volume and plasma Na by inhibiting prostaglandin synthesis.
137
How do you treat hypernatraemia
Correct water deficit if dehydrated with 1L 5% dextrose IV over 8-10h
treat cause
138
complications of hypernatraemia
RAPID HYPERnatraemia correction> cerebral oedema
139
causes of HYPONATRAEMIA (by fluid status)
HYPOVOLAEMIC:
- diarrhoea
- vomiting
- diuretics
EUVOLAEMIC: (E=endocrine)
- SIADH
- Hypothyroid
- Adrenal insufficiency
HYPERVOLAEMIA: (overloaded = organ failure)
- liver failure
- CCF
- renal failure
140
what occurs physiologically in the kidneys if hypovolaemic and how does it affect sodium concentration?
kidneys increase sodium reeabsorption
this draws in water
this decreases urinary sodium
141
How can we interpret urinary sodium in the context of hyponatraemia
urinary sodium LOW: this is due to hypovolaemic state (kidneys functioning as normal)
urinary sodium HIGH (above 20): SIADH
142
what are the two hormones that regulate sodium absorption
aldosterone
| ADH
143
how does aldosterone work
bids to Mineralocorticoid R
| Increases NA reabsorption> pulls in water
144
how does ADH work
inserts aquaporin channels > water reabsorption
145
what mx required in hyponatraemia?=
* HYPOVOLAEMIC: IV 0.9% saline slowly
* Euvolaemic / HYPERvolaemic: fluid restrict (0.5-1L) + treat cause
* ACUTE SEVERE hyponatraemia <120 : IV 3% isotonic saline
146
what do you do if patient is severely hyponatramemiic (<120)
slow 3% ISOTONIC saline
147
what drugs can you give for SIADH
Demeclocycline (induce nephrogenic DI, reducing responsiveness of collecting tubes to ADH )
Tolvaptan (V2 receptor antagonist)
148
what ix do you do for SIADH
plasma osmolarity and urine osmolarity
| plasma will be low, urine will be high
149
complication of treating hyPOnatraemia too fast
cerebral POntine myelinolysis (patients are awake but cannot move or speak ~ Locked in syndrome)
150
Causes of HYPERkalaemia
DECREASED RENAL POTASSIUM EXCRETION
- Low GFR (poor kidney functon> insufficient K excreton)
- Low renin (T24 RTA, NSAIDS)
- ACEi
- ARBs
- Addison's (no aldosterone > no K+ excretion)
- Aldosterone antagonist (counters aldosterone effect, eg spironolactone)
INCREASED POTASSIUM RELEASE FROM CELLS
- rhabdo
- acidosis
151
summartise drugs that cause HYPERKALAEMIA
NSAIDS
ACE i
ARBs
Spironolactone
152
Whhat is presentation of hyperkalaemic pt
muscle weakness and lethargy
fatigue
parasthesia
palpitations
153
ECG in hyperkalaemia
```
TALL N TENTED T WAVE
Broad QRS
Flat P wave
Prolonged PR interval
Eventual SINE WAVE > > cardiac arrest
```
154
causes of HYPOKALAEMIA
- GI loss (diarrhoea)
- renal loss (loop and thiazide diuretics, excess MR with Conns, Cushings)
- redistribution into cells (insulin / insulinomas, beta agonists, alkalosis)
155
mx hypokalaemia
K+ >2.5: 2 sandoK tablets TDS for 48h
| K+ <2.5 or symptoms /ECG: 3x 1L NaCl with 40mmol KCL over 24h
156
sick euthyroid cause
acute illness -- abnormal thyroidd results but will normalise oncee illness resolves
157
sick euthyroid biochemistry
Normal or low TSH
| low T3 and T4
158
how do you investigate acromegaly
serum IGF1
to confirm dx, do an OGTT with GH measurement
159
what do you need to give in refeeding syndrome
phosphate
160
causes of SIADH
CNS pathology - stroke, haemorrhage, tumour
Lung pathology - pneumonia, pneumothorax
Drugs - SSRI, TCA, carbamazepine, sulphonylurea
Tumour
Surgery
161
what occurs with SIADH
Excess ADH > increased water retention > increased volume >RAAS suppressed > less aldosterone > less water absorption
So HYPOnatraemia with EUvolaemia
162
how do you treat MODY
MODY is very sensitive to sulphonylureas
163
what is carinoid syndrome
- neuroendocrine tumour --> Releases serotonin & other vasoactive peptides (histamine, bradykinin, prostaglandins) into systemic circulation --> serotonin syndrome
- can also secrete pit hormones (**ACTH**) --> **cushingoid** and **hypok and hyperna** (when high concs of cortisol)
164
aetiology of carcinoid syndrome
Metastasis of carcinoid tumour to liver → ↓metabolism of serotonin by liver → symptomatic carcinoid syndrome
165
what does serotonin do in carcinoid syndrome
↑gut motility & peristalsis, vasoconstriction, endocardial fibrosis
166
carcinoid syndrome rf
MEN1
167
Symptoms of carcinod syndrome
* Diarrhoea
* Facial flushing
* Bronchospasm → wheeze, SOB
* Palpitations
* Abdominal cramps
168
key investigation for carcinoid syndrome
* ↑urinary 5-hydroxyindoleacetic acid (5HIAA)
169
management of carcinoid syndrome
* 1st line = surgical resection (local + node clearance)
* medical = somatostatin analogues e.g. octreotide (inhibits serotonin release)
170
define hypoglycaemia
blood glucose < 3.5 mmol/L
171
hypoglycaemia risk factors
1. Insulin-dependent diabetes
2. Previous hx of hypoglycaemic episodes
3. Impaired renal function
4. Cognitive dysfunction/dementia
5. Alcohol misuse
6. Profound starvation
7. Increased exercise
172
investigations for hypoglycaemia
1. **Bedside**: obs, ECG, ABG, capillary blood glucose
* ECG as MI may be precipitated by hypoglycaemia
2. **Bloods**: FBC, U&E, CRP, serum glucose, ketones
3. **Imaging**: may need CT head if intracranial pathology suspected, after discussion with senior
173
initial management of hypoglycaemia
* airway: manage if low GCS
* Breathing: Oxygen if SaO2 low
* Circulation: Fluid resuscitation if hypovolaemic (500ml bolus of 0.9% sodium chloride over 15 mins or 250ml bolus if increased risk of fluid overload e.g. HF
o Reassess after each bolus for fluid balance
o Repeat boluses up to 4 times --> sernior input if
negative response (e.g. increased chest crackles i.e. fluid overload) or patient not responding to boluses (i.e. persistent hypotension)
174
management to reverse hypoglycaemia
* If *conscious and able to swallow*: 1**0-20g fast-acting carbohydrate** (e.g 2-4 heaped teaspoons sugar dissolves in water)
* If *drowsy/confused but swallow intact*: **Buccal glucose gel (e.g. Hypostop/glucogel**) ~ sublingual
* * If unconscious or concern about swallow*:
- If **no IV access: IM 1mg glucagon**
- If **IV access or no response **after 10 minutes: **10% IV glucose 150ml **
175
driving advice for hypogylcaemia
to drive a car must not have had **> 1 episode of hypoglycaemia ** requiring assistance of another person in ** preceding 12 months ** --> tell DVLA
176
when should SGLT-2 be added to metformin
if patient at risk of CKD or chronic heart failure, QRISK > 10%
