Endocrinology Flashcards
1
Q
Define DIABETES MELLITUS
A
- Chronic hyperglycemia due to insulin dysfunction
- can’t move glucose from blood into cells
- low glucose in cells so they starve of energy
2
Q
epidemiology of TYPE 1 DIABETES MELLITUS
A
- early onset <30 yrs old
- usually lean
- northern european ancestry
3
Q
epidemiology of TYPE 2DIABETES MELLITUS
A
- older onset >30 yrs
- overweight
- common in african/asian people
4
Q
list 8 risk factors for TYPE 2 DIABETES MELLITUS
A
Modifiable
1) . obese
2) . hypertension
3) . hyperlipidemia
4) . drinking excess alcohol
5) . sedentary lifestyle
Non-modifiable
1) . older
2) . family history
3) . asian/african heritage
5
Q
list 3 causes of TYPE 1 DIABETES MELLITUS
A
- HLA DR3/4 (cell surface receptors) affected in >90% of people
- autoimmune disease which targets islet cells
- family history
6
Q
list 5 potential cause of TYPE 2 DIABETES MELLITUS
A
- pancreatic (pancretitis, surgery, trauma, destruction, cancer)
- cushing’s disease
- acromegaly
- hyperthyroidism
- pregnancy
7
Q
outline the general pathology of TYPE 1 DIABETES MELLITUS
A
- Autoimmune destruction of pancreatic B-cells in Islets of Langerhans
- Associated with HLA genetics
8
Q
explain the pathology of polyuria in TYPE 1 DIABETES MELLITUS
A
- blood glucose exceeds the renal tubular reabsorptive capacity
- leads to osmotic diuresis (increased urination rate)
9
Q
explain the pathology of weight loss in TYPE 1 DIABETES MELLITUS
A
- fluids have been depleted + insulin deficiency
- leads to muscle and fat breakdown
10
Q
briefly outline the pathology of TYPE 2 DIABETES MELLITUS
A
- B-cell mass reduced to 50% of normal
- low insulin secretion + peripheral insulin resistance
- beta cell hypertrophy + hyperplasia to create more insulin to remove glucose from blood
11
Q
what is the length of history you assess for in TYPE 1 DIABETES MELLITUS
A
2-6 weeks
12
Q
list 4 signs / symptoms for TYPE 1 DIABETES MELLITUS
A
- polydipsia (excessive thirst)
- polyuria (excessive urination)
- weight loss
- polyphagia (excess appetite)
13
Q
if TYPE 1 DIABETES MELLITUS is not picked up fast, what is another symptom and what does it indicate
A
- fruity breath -> indicates KETOACIDOSIS
14
Q
explain the pathology of polydipsia in TYPE 1 DIABETES MELLITUS
A
- excessive thirst
- due to fluid / electrolyte loss
15
Q
list 4 signs/symptoms for TYPE 2 DIABETES MELLITUS
A
usually >asymptomatic< BUT…
- Central obesity
- elevated cholesterol
- elevated triglycerides
- raised BP
16
Q
list 2 investigations for TYPE 1 DIABETES MELLITUS
A
- Fasting plasma glucose
- random plasma glucose
17
Q
what should be the results of the FASTING plasma glucose in TYPE 1 DIABETES MELLITUS
A
> 7.0 mmol/L
18
Q
what should be the results of the RANDOM plasma glucose in TYPE 1 DIABETES MELLITUS
A
> 11.1 mmol/L
19
Q
what is required for a diagnosis of TYPE 1 DIABETES MELLITUS
A
Symptoms of hyperglycemia + 1 or more of:
- ketosis
- rapid weight loss
- age of onset <5 yrs old
- BMI < 25KG/M²
20
Q
outline the management of TYPE 1 DIABETES MELLITUS
A
- insulin twice daily with meals
- glycaemic control via diet -> low sugar/fat foods
21
Q
list 4 investigations for TYPE 2 DIABETES MELLITUS
A
- HbA1C
- random blood glucose
fasting blood glucose - oral glucose tolerance test (GTT) 2 hrs post meal
22
Q
briefly describe the HbA1C test
A
- tests proportion of Hb in RBC that has a glucose on it (glycated haemoglobin)
- gives indication of how long blood glucose levels have been high
23
Q
expected result for FASTING plasma glucose in suspected TYPE 2 DIABETES MELLITUS
A
> 7mmol/L
24
Q
expected result for RANDOM plasma glucose in suspected TYPE 2 DIABETES MELLITUS
A
> 11.1mmol/L
25
expected result for oral GTT 2 hrs post meal in suspected TYPE 2 DIABETES MELLITUS
>11.1mmol/L
26
expected result for HbA1c in suspected TYPE 2 DIABETES MELLITUS
>47mmol/L
| >6.4%
27
list 4 scenarious where you wouldn't use HbA1c
- pregnancy
- children
- T1DM
- pancreatic surgery
28
list 3 diagnostic criteria combinations for TYPE 2 DIABETES MELLITUS
1) symptoms of hyperglycemia + 1 abnormal glucose result
2) asymptomatic + 2 separate abnormal glucose results
3) abnormal HbA1c
29
outline 4 non-pharmacological management of TYPE 2 DIABETES MELLITUS (try these before giving drugs)
- diet excercise changes
- patient education
- smoking cessation
- regular blood glucose monitoring using HbA1c
30
outline the pharmacological treatment pathway for TYPE 2 DIABETES MELLITUS
1st line)
- Biguanide (METFORMIN)
2nd line)
* metformin AND*
- sulphonylurea
- DPP4 inhibitor
- pioglitazone
3rd line)
- insulin
31
Drug class - BIGUANIDE. Give an example.
METFORMIN
32
Drug class - BIGUANIDE. Give mechanism of action
- reduce gluconeogenesis in liver (this is increased in T2DM bc of excess glucagon)
- increased uptake/utilisation of glucose in skeletal muscle (increased insulin sensitivity)
33
Drug class - BIGUANIDE. give contraindications
- people with renal (main one) / liver problems
34
Drug class - BIGUANIDE. give side effects
1) . GI disturbance (leads to weight loss!!)
- abdo pain
- anorexia
- diarrhoea
- nausea
2) . lactic acidosis (rare) in:
- renal disease
- liver disease
35
Drug class - SULPHONYLUREA. give 2 examples
- gliclazide
| - glipizide
36
Drug class - SULPHONYLUREA. give mechanism of action
- stimulate B cells to secrete more insulin
37
Drug class - SULPHONYLUREA. give contraindications
- pregnancy / breastfeeding -> can cross the placenta and enter breast milk
- may cause hypoglycemia in newborns
38
Drug class - SULPHONYLUREA. give side effects
- hypoglycemia
| - weight gain (stimulates appetite)
39
Drug class - DPP4 INHIBITORS. give example
Stigaliptin
40
Drug class - DPP4 INHIBITORS. Give mechanism of action
- inhibit DPP4 -> stopping breakdown of incretins GLP-1/GIP
- GLP-1/GIP stimulate insulin secretion
*DPP4 normally inhibits incretins*
41
Drug class - THIAZOLIDINEDIONES. give example
proglitazone
42
Drug class - THIAZOLIDINEDIONES. give mechanism of action
- enhance fatty acid / glucose uptake -> body makes more fat from these
43
Drug class - THIAZOLIDINEDIONES. give side effects
- fluid retention
| - weight gain
44
what might you also give DIABETICS so they have cardiovascular protection?
- statins
| - antihypertensives
45
list 7 DIABETIC complications
1) diabetic nephropathy
2) diabetic neuropathy (lack of foot sensation -> ulcers etc)
3) diabetic retinopathy (blood shot eyes -> sight loss)
4) erectile dysfunction
5) arterial disease (IHD / MI)
6) Staph skin infections
7) Diabetic ketoacidosis
46
HYPOGLYCAEMIA - aetiology
insufficient glucose to brain
47
HYPOGLYCAEMIA - cause
complication of insulin of sulfonylurea therapy
48
HYPOGLYCAEMIA - whats the blood glucose threshold
below 3mmol/L
49
HYPOGLYCAEMIA - list 5 signs and symptoms
1) . odd behaviour (aggression)
2) . sweating
3) . tachycardia (fast HR)
4) . hunger
5) . pallor (unhealthily pale)
50
HYPOGLYCAEMIA - how would you diagnose
blood glucose level test
51
HYPOGLYCAEMIA - 2 ways you would manage
- glucose (IV/Food)
| - glucagon
52
DIABETIC KETOACIDOSIS - what is it
- state of uncontrolled hyperglycemia and catabolism (breakdown)
- associated with insulin deficiency
53
DIABETIC KETOACIDOSIS - outline the general pathophysiology
1) . no insulin so LOTS of hepatic gluconeogensis
2) . lots of glucose -> osmotic diuresis -> dehydration
3) . peripheral lipolysis -> increased FFAs -> converted to acidic ketones in liver
4) . ketones increase acidity of blood -> metabolic acidosis
54
DIABETIC KETOACIDOSIS - list 7 clinical features
1) . dehydration
2) . vomiting / abdo pain
3) . sunken eyes / dry tongue
4) . Kussmaul's breathing
5) . fruity breath (ketone smell)
6) . low BP
7) . low temp
55
DIABETIC KETOACIDOSIS - what's Kussmaul's breathing
- deep and rapid breathing
| - resp compensation for the metabolic acidosis
56
DIABETIC KETOACIDOSIS - how would you diagnose (4 things)
- ketones raised
- blood glucose >11mmol/L
- blood pH <7.3
- blood bicarb <15
57
DIABETIC KETOACIDOSIS - list 3 treatments
- fluid replacement -> 0.9% NaCl (saline)
- IV insulin
- electrolytes (k+)
58
HYPEROSMOLAR HYPERGLYCAEMIC STATE - what is it
- complication of DM - high blood sugar -> high osmolarity (lots of particles in solution)
- little/no ketoacidosis
59
HYPEROSMOLAR HYPERGLYCAEMIC STATE - what causes it
infection, especially pneumonia
60
HYPEROSMOLAR HYPERGLYCAEMIC STATE - list 3 clinical features
- dehydration (from osmotic diuresis)
- reduced consciousness (from conc. plasma)
- polyuria
61
HYPEROSMOLAR HYPERGLYCAEMIC STATE - how to diagnose
blood glucose test
62
HYPEROSMOLAR HYPERGLYCAEMIC STATE - list 4 treatments
1) . low molecular weight heparin (hyperosmolality makes blood thick so reduces clots / MI / stroke risk)
2) . fluid replacement 0.9% NaCl
3) . insulin
4) . electrolytes (k+)
63
Define HYPOTHYROIDISM
Reduced action of thyroid hormone
64
define PRIMARY HYPOTHYROIDISM
- decreased levels of T4
| - issue with thyroid gland
65
define SECONDARY HYPOTHYROIDISM
- decreased TSH
| - pituitary / hypothalamic issue
66
list 4 causes of PRIMARY HYPOTHYROIDISM
1) . Primary atrophic hypothyroidism
2) . Hashimoto's Thyroiditis (autoimmune)
3) . Drugs -> post-thyroidectomy/radioiodine/antithyroid
4) . lithium/amiodarone
67
list 4 causes of SECONDARY HYPOTHYROIDISM
1) . hypopituitarism (neoplasm, infection)
2) . isolated TSH deficiency
3) . hypothalamic disorders (neoplasms, trauma)
4) . iodine deficiency
68
outline the pathology of PRIMARY HYPOTHYROIDISM
- aggressive autoimmune destruction of thyroid cells
| - antibodies bind and block TSH receptors -> inadequate thyroid hormone made/secreted
69
outline the pathology of SECONDARY HYPOTHYROIDISM
- release + production of TSH is decreased
| - therefore reducd T3/T4 released
70
list 10 symptoms of HYPOTHYROIDISM
* everything down*
1) . hoarse voice
2) . constipation
3) . COLD intolerance
4) . weight GAIN
5) . menorrhagia (heavy period)
6) . myalgia (muscle pain)
7) . weakness
8) . tired
9) . LOW mood
10) . dementia
71
list the 11 signs of HYPOTHYROIDISM (think BRADYCARDIC)
```
Bradycardic(slow HR)
Reflexes relax slowly
Ataxia
Dry thin hair/skin
Yawning (drowsy/coma)
Cold hands
Ascites (abdo fluid buildup)
Round puffy face
Defeated demeanour
Immobile
Congestive heart failure
```
72
list 4 investigations for HYPOTHYROIDISM
1) . thyroid function test
2) thyroid antibodies
3) . lipids/cholesterol
4) . FBC
73
what would thyroid function test show in suspected HYPOTHYROIDISM
Primary - high TSH / low free T4
Secondary - low TSH / low T3/T4
74
what would thyroid antibody test show in suspected HYPOTHYROIDISM
thyroid antibodies present
75
what would FBC / cholesterol test show in suspected HYPOTHYROIDISM
FBC
- anaemia
- macrocytic anaemia in women due to menorrhagia
cholesterol
- hyperlipidemia
76
outline the management of HYPOTHYROIDISM
- Levothyroxine (T4 replacement)
Primary -> remove thyroid growth (goitre)
Secondary -> treat underlying cause (TSH may always be low)
77
define HYPERTHYROIDISM (thyrotoxicosis)
Overactivity of the thyroid gland -> excess thyroid hormone
78
list 6 causes of HYPERTHYROIDISM
1) . Graves' disease (most common)
2) . toxic multinodular goitre
3) . toxic thyroid adenoma
4) . pituitary adenoma
5) . De Quervain's thyroiditis
6) . Iatrogenic -> iodine/amiodarone/lithium
79
what is De Quervain's thyroiditis
- short lasting hyperthyroidism
- accompanied by:
1) .fever
2) .malaise
3) .neck pain
- treat with aspirin
- give prednisolone if severe
80
list 9 symptoms of HYPERTHYROIDISM
* everything UP*
1) . Palpitations
2) . diarrhoea
3) . HEAT intolerant
4) . weight LOSS
5) . INCREASED appetite
6) . oligomenorrhea
7) . tremor
8) . irritable
9) . Labile emotion (volatile)
81
list 11 signs of HYPERTHYROIDISM (6 categories)
```
HANDS - moist/warm/red palms
PULSE - tachycardic/AF
FACE - thin hair
NECK - Goitre/nodules/bruit
SWEATING
HYPERREFLEXIA
```
82
list 4 investigations for suspected HYPERTHYROIDISM
1) .Thyroid function tests
2) . thyroid autoantibodies
3) . thyroid ultrasound
4) . radioactive iodine isotope uptake scan
83
what would be the results of TFTs in suspected HYPERTHYROIDISM
Primary
- low TSH
- high T3/T4
Secondary
- high TSH
- high T3/T4
84
what would be the results of thyroid autoantibodies in suspected HYPERTHYROIDISM
- TPOs more often seen in HYPOTHYROIDISM
- thyroglobulin antibodies seen
- TSH receptor antibody (TRAb) in GRAVES'
85
what would be the results of radioactive iodine uptake scan in HYPERTHYROIDISM
- much greater uptake of iodine in GRAVES'
86
list 4 treatments HYPERTHYROIDISM
1) . beta blockers
2) . anti-thyroid drug
3) . radioiodine therapy
4) . thyroidectomy
87
drug class - BETA BLOCKER. give example + method of action
- PROPRANOLOL
- rapidly controls symptoms
- decreases Sympathetic Nervous System (SNS)
88
drug class - ANTI-THYROID. give example + method of action
- CARBIMAZOLE
- blocks thyroid hormone synthesis
- has immunosuppressive effects which affect GRAVES'
89
Contraindications and side effects of RADIOIODINETHERAPY
CI
- pregnancy
- breast feeding
SE
- Lead to HYPOTHYROIDISM
90
list 3 potential complications of THYROIDECTOMY
1) bleeding
2) post-op infection
3) hypothyroidism
91
define GRAVES' disease
- hyperthyroidism
| - due to pathological stimulation of TSH receptor
92
list a cause of GRAVES'
- autoimmune disease
| - associated with mysthenia gravis
93
list 5 signs / symptoms of GRAVES'
1) . increased HR
2) tremor
3) NECK - goitre/brut
4) EYES - bulging out/proptosis
5) Thyroid ACROPACHY (swelling of hands/feet)
94
Investigation for GRAVES'
TFTs
- high T3/T4
- Low TSH
95
outline management for GRAVES'
*same as HYPERTHYROIDISM*
1) . Beta blocker
2) . anti-thyroid drug
3) . thyroidectomy
4) radioiodine therapy
96
define HASHIMOTO'S THYROIDITIS
- hypothyroidism
| - due to aggressive thyroid cell destruction
97
epidemiology of HASHIMOTO'S THYROIDITIS (3 things)
1) . 12-20x more common in women
2) . most common cause of goitrous hypothyroidism
3) . associated with other autoimmune conditions
98
cause of HASHIMOTO'S THYROIDITIS + 3 triggers
*autoimmune*
Triggers
1) . iodine
2) . infection
3) . smoking
99
pathology of HASHIMOTO'S THYROIDITIS
1) . aggressive autoimmune destruction of thyroid cells
2) . antibodies bind and block TSH receptors
3) . blocking leads to inadequate thyroid hormone production/scretion
100
list 4 signs / symptoms of HASHIMOTO'S THYROIDITIS
1) hypothyroid symptoms
2) . rapidly enlarged thyroid gland
3) . dyspnoea / dysphagia (from neck pressures)
4) . Goitre
101
list 2 investigations and what you'd see in suspected HASHIMOTO'S THYROIDITIS
1) . TFTs
- TSH raised
2) . Thyroid antibodies
- present
102
3 ways to manage HASHIMOTO'S THYROIDITIS
*same as hypothyroidism*
1) . levothyroxine
2) . remove goitre
3) . treat underlying cause
103
list 5 thyroid cancers in order of prevalence
* all different cell types*
1) . papillary
2) . follicular
3) . medullary
4) . lymphoma
5) . anaplastic
104
describe the behaviour/spread/prognosis for PAPILLARY
B). usually effects young people
S). local
P). good
105
describe the behaviour/spread/prognosis for FOLLICULAR
B). effects middle aged people
S). lung/bone
P). usually good
106
describe the behaviour/spread/prognosis for MEDULLARY
B). often familial
S). local and metastases
P). poor
107
describe the behaviour/prognosis for LYMPHOMA
B). variable
| P). usually poor
108
describe the behaviour/spread/prognosis for ANAPLASTIC
B). aggressive
S). local
P). very poor
109
list 2 signs/symptoms of:
- PAPILLARY
- FOLLICULAR
- ANAPLASTIC
1) . hard fixed nodule
| 2) . enlarged lymph nodes on examination
110
list a sign/symptom of LYMPHOMA
rapidly growing mass in neck
111
list 3 signs/symptoms of MEDULLARY
1) . diarrhoea
2) . flushing episodes
3) . itching
112
what is the differential for THYROID CANCERS
goitre
113
investigation for THYROID CANCERS
- fine needle aspiration (biopsy)
114
what is the management for:
- PAPILLARY
- FOLLICULAR
TOTAL thyroidectomy (remove whole gland)
115
what is the management for:
- ANAPLASTIC
- LYMPHOMA
Radiotherapy for palliative care
116
list 2 managements for:
| - MEDULLARY
1) . TOTAL thyroidectomy
| 2) . central lymph node dissection
117
define CUSHING'S SYNDROME
- persistently elevated glucocorticoid in circulation (CORTISOL)
118
where is cortisol released
Zona Fasciculata of adrenal gland
119
epidemiology of CUSHING'S
- 2/3rds of cases = Cushing's Disease
| - increased incidence in diabetes
120
list the types of causes for CUSHING'S syndrome
1) . ACTH dependant
| 2) . ACTH independent
121
list 3 causes of ACTH Dependant disease
*increased Adrenocorticotropic*
1) . excessive ACTH from pituitary adenoma (CUSHING'S DISEASE)
2) . ACTH producing tumour
3) excess ACTH administration
122
list 3 causes of ACTH independent disease
* decreased adrenocorticotropic*
1) . adrenal adenoma/carcinoma
2) . adrenal nodular hyperplasia
3) . excess glucocorticoid administration (iatrogenic -> hydrocortisone)
123
what is CUSHING'S DISEASE
cushing's syndrome but cause is PITUITARY ADENOMA
124
outline the pathology of CUSHING'S SYNDROME
1) . lots of features bc cortisol is catabolic -> thin skin / easy bruising / striae
2) . excessive alcohol mimics signs (pseudo-cushing's) -> fixed with alcohol recession
3) . loss of normal feedback mechanisms / loss of circadian rhythm
125
list 6 symptoms of CUSHING'S SYNDROME
1) . acne
2) . weight GAIN
3) . gonadal dysfunction (irregular menses/hirsutism/virilisation)
4) . weakness
5) . mood change
6) . recurrent achilles injury
126
briefly outline the gonadal dysfunction seen in CUSHING'S SYNDROME
1) . irregular menses (periods)
2) . hirsutism -> hair growing where it shouldn't
3) . virilisation -> male characteristics developing in a female or too early in a boy
127
list 10 signs of CUSHING'S SYNDROME (3 categories)
FAT DISTRIBUTION
- central obesity
- moon face
- buffalo neck hump
- supraclavicular fat
SKIN CHANGES
- thin skin
- bruising
- purple abdo striae
OTHER
- osteoporosis
- red face
- muscle atrophy
128
outline investigation pathway for CUSHING'S SYNDROME
1) . confirm raised cortisol
| 2) . establish cause (do plasma cortisol)
129
CUSHING'S SYNDROME - investigations to confirm raised cortisol
1) . overnight dexamethasone suppression test (shows no suppression)
2) . 48 hour low-dexamethasone suppression test (shows urinary free cortisol elevated)
130
CUSHING'S SYNDROME - investigations to establish cause
*PLASMA CORTISOL (synacthen)*
1) . if ACTH undetectable
- susp adrenal tumour
- CT adrenal glands
- if no mass -> adrenal vein sampling
2) . if ACTH detectable
- pituitary issue or ectopic
- high dose dexamethasone suppression test (pituitary causes suppression)
- CRH test (cortisol rises with pituitary)
131
outline the 5 treatment pathways for CUSHING'S SYNDROME
1). stop steroids (iatrogenic)
2). adrenalectomy (adrenal adenoma)
adrenalectomy + radiotherapy + adrenolytic drugs (adrenal carcinoma)
3) trans-sphenoidal surgery / bilateral adrenalectomy (Cushing's disease)
4) . cortisol synthesis inhibition drugs
5) . surgery to remove tumour (ectopic)
132
list 3 drugs which bring down cortisol levels
1) metyrapone
2) ketoconazole
3) fluconazole
133
explain the risk of an adrenalectomy
*may cause NELSON'S SYNDROME*
- adrenals removed = no cortisol to respond to ACTH
- no cortisol = no negative feedback loop for ACTH
- ACTH builds up in tissues
FEATURES
- bronze skin
- visual disturbance
- headache
134
define ACROMEGALY
- overgrowth of all organ systems
| - due to excess growth hormone
135
epidemiology of ACROMEGALY
- avg age = 40
| - 5% association with MEN-1 (hereditary endo tumours)
136
list 3 causes of ACROMEGALY
1) . excessive GH secretion via pituitary tumour
2) . other GH releasing tumours (hypothalamus/lung)
3) . hyperplasia
137
outline the pathology of ACROMEGALY
- GH acts directly on tissues ie. liver/bone/muscle
- GH acts indirectly via induction of IGF-1 (insulin-like growth factor)
- excess causes uncontrolled growth
138
how can GIGANTISM occur
if ACROMEGALY present in children before epiphyseal plates fuse
139
list 8 symptoms of ACROMEGALY (slow onset)
1) . snoring
2) . deep voice
3) . increased sweating
4) . weight GAIN
5) . reduced libido
6) . amenorrhoea
7) . back pain
8) . acroparesthesia (burning/tingling in extremities when you wake up)
140
list 6 signs of ACROMEGALY
1) skin darkening - acanthosis nigricans
2) prognathism (jaw protrudes)
3) . interdental separation (gap teeth)
4) . macroglosia (huge tongue)
5) . spade hands/feet
6) . carpal tunnel syndrome
141
list 4 investigations and what you'd expect to see in ACROMEGALY
1) . oral GTT = GH high after given glucose
2) . serum IGF-1 = raised IGF-1
3) . MRI pituitary fossa = evidence of pituitary adenoma
4) . visual field test = bitemporal hemianopia
142
why shouldn't you rely on just a random Growth Hormone test for ACROMEGALY
- GH has pulsatile secretion
| - levels vary throughout the day
143
outline the 1st/2nd/3rd line management for ACROMEGALY
1st line
- transphenoidal resection surgery (removes adenoma / corrects surroundings)
2nd line
- somatostatin analogues
(octreotide)
3rd line
- GH receptor antagonists
(pegvisomant)
144
list 3 complications of ACROMEGALY
1) . hypertension
2) . diabetes
3) . untreated can impact optic chiasm -> blindness
145
define CONN'S SYNDROME (primary hyperaldosteronism)
- high aldosterone levels
- independant of RAAS
- Na / water retention
146
list 2 causes of CONN'S SYNDROME
1) . adrenal adenoma -> secreting aldosterone
| 2) . bilateral adrenal hyperplasia
147
outline the pathology of CONN'S SYNDROME
1) aldosterone causes Na/K exchange in distal renal tubule
2) . therefore hyperaldosteronism causes increased Na/water resorption
- and also causes increased K excretion
3) . reduced renin release
148
list 6 signs and symptoms for CONN'S SYNDROME
* HYPOKALAEMIC signs*
1) . cramps
2) . alkalosis
3) . weakness
4) . hypertension
ALSO
1) . low urine output
2) . paraesthesia(pins/needles)
149
outline the 3 tests for CONN'S SYNDROME and what each would show
U&E's
1) decreased renin
2) increased aldosterone
3) Na = UP
4) K = DOWN
ECG
1) flat T wave
2) ST depression
3) long QT
4) long PR
5) pathological U wave
Adrenal CT/MRI
- confirmation of aldosterone producing adenoma
150
outline the 2 treatments for CONN'S SYNDROME
if ADENOMA
- laparascopic adrenalectomy
if HYPERPLASIA
- aldosterone antagonist
( spironolactone)
151
define ADDISON'S DISEASE
- primary adrenocortical insufficiency
- destruction of adrenal cortex
- decrease in gluco/mineralocorticoids/androgens
152
outline the pathology of ADDISON'S DISEASE
1) . destruction of adrenal cortex
2) . less cortical produced
3) . excess ACTH stimulates melanocytes
4) . hyperpigmentation
153
list 4 causes of ADDISON'S DISEASE
1) . autoimmune adrenalitis
2) . adrenal TB
3) . surgical removal of adrenals
4) . adrenal metastases
154
list 12 symptoms of ADDISON'S DISEASE (4 categories)
*Tanned, tired, toned, tearful*
GI
1) . nausea/vomiting
2) . abdo pain
3) . constipation/diarrhoea
4) . anorexia
BODY
1) . tanned skin
2) . lean -> weight loss
NEURO
1) . weakness
2) . confusion
3) . syncope (faint)
OTHER
1) . myalgia (tired muscles)
2) . depression
3) . malaise (discomfort)
155
list 8 signs of ADDISON'S DISEASE (3 categories)
HYPERPIGMENTATION
1) . palmar creases
2) . buccal mucosa (brown mouth)
3) . vitiligo (patchy skin)
CARDIO
1) . postural hypotension (BP drops when stood up)
2) . shock BP up/HR down/coma
OTHER
1) . dehydration
2) . general wasting
3) . alopecia
156
outline the 4 investigations and what you'd see for ADDISON'S DISEASE
1) . ACTH stimulation test
- cortisol stays low after giving ACTH (synACTHen)
2) . plasma ACTH
- HIGH = primary hypoaldosteronism
- LOW = secondary/tertiary hypoaldosteronism
3) . U&E
- high renin
- low aldosterone
- low Na
- high K
- high urea
4) . adrenal antibodies
- 21-hydroxylase present
157
outline the 3 treatments for ADDISON'S DISEASE
1) . Replace glucocorticoids (cortisol) with Hydrocortisone/Prednisolone
2) . replace mineralocorticoids (aldosterone) with fludrocortisone
3) . double dose of steroids if infection/trauma/surgery
158
what is the function of potassium K+
maintains resting potential of all muscles in body
159
give 3 ways that serum potassium K+ is controlled
1) . uptake of K+ into cells
2) . renal excretion (aldosterone)
3) . GI loss
160
define HYPERKALEMIA
abnormally high potassium K+ in blood
161
list 5 causes of HYPERKALEMIA (think DREAD)
```
Drugs (ACE-i/K+ sparing diuretics)
Renal failure
Endocrine (Addison's)
Artefact (consider ECG)
DKA (or other acidosis)
```
162
outline the pathology of HYPERKALEMIA
1) . K+ in blood determines excitability of nerve and muscle cells including heart
2) . when K+ rises -> reduced electrical potential btwn cardiac myocyte/outside cell
3) . threshold for action potential decreased
4) . abnormal action potential -> arrhythmias -> cardiac arrest
163
list 6 Symptoms + 2 Signs of
| HYPERKALEMIA
SYMPTOMS
1) . usually asymptomatic til reaches MI
2) . muscle weakness
3) . impaired neuromuscular transmission
4) . flaccid paralysis
5) . light headed
6) . chest pain
SIGNS
1) . tachycardia
2) . Kussmaul's breathing (from metabolic acidosis)
164
outline 2 investigations for HYPERKALEMIA and what you would see
U&Es
>5.5mmol/L = hyperkalaemic
>6.5mmol/L = emergency
ECG
- tall tented T waves
- Small P waves
- Wide QRS complex
165
outline 4 treatments for MILD HYPERKALEMIA
1) . treat underlying cause
2) . dietary Potassium restriction
3) . restrict hypokalaemic drugs
4) . loop diuretic
166
example of loop diuretic and how it works
- FUROSEMIDE
| - increases urinary k+ excretion
167
outline 1st/2nd/3rd line treeatment for SEVERE HYPERKALEMIA (medical emergency)
1st) . Calcium Gluconate (stabilise cardiac membrane)
2nd) . insulin + dextrose (drive K+ into cells)
3rd) . polystyrene sulfonate resin (binds K+ in gut = decreased uptake)
168
define HYPOKALEMIA
deficiency of potassium K+ in blood stream
169
outline tha pathology of HYPOKALEMIA
1) . low K+ in serum (ECF)
2) . causes water conc. grad out of cell (ICF)
3) . increased leakage from ICF
4) . cardiac myocyte membrane hyperpolarised
5) . monocyte excitability decreased
170
list 5 causes of HYPOKALEMIA
1) . fasting
2) . anorexia
3) . high renal aldosterone (aldosterone stimulates K+ excretion)
4) . increased renal excretion (loop diuretics)
5) . GI loss (vomiting/diarrhoea)
171
list 5 signs/symptoms of HYPOKALEMIA
*usually asymptomatic*
1) . muscle weakness
2) . cramps
3) . tetany (intermittent muscle spasms)
4) . palpitations
5) . constipation
172
list 2 investigations and their findings for HYPOKALEMIA
U&E (serum K+)
<3.5mmol/L = hypokalaemia
<2.5mmol/L = emergency
ECG
1) . U waves
2) . small/inverted T
3) . ST depression
4) . long PR
5) . long QT
173
outline the treatment for mild and severe HYPOKALEMIA
MILD
- Oral K+ (sando-K)
- K+ sparing diuretic (spironolactone)
SEVERE
- IV K+
174
define SYNDROME OF INAPPROPRIATE ADH (SIADH)
- continued ADH secretion
| - despite plasma hypotonicity and normal plasma volume
175
what's the generalised cause of SIADH
- disordered hypothalamic-pituitary secretion
| - ectopic production of ADH
176
List 3 Neuro causes of SIADH
1) tumour
2) trauma
3) meningitis
177
List 3 Pulmonary causes of SIADH
1) .Cystic Fibrosis
2) . Asthma
3) . Pneumonia
178
List 4 Drug causes of SIADH
1) . opiates
2) . carbamazepine
3) . chloropropamide
4) . vincristine
179
List 4 Malignancy causes of SIADH
1) . small cell lung carcinoma
2) . prostate
3) .thymus
4) pancreas
180
outline the pathology of SIADH
excess ADH -> more aquaporin 2 inserted -> water retention -> excess blood volume -> hyponatremia (via dilution)
181
list 5 symptoms for SIADH
1) . Reduced GCS (confused/drowsy)
2) . irritable
3) . headaches
4) . anorexia
5) . Nausea
182
list 2 signs of SIADH
1) . conc urine
| 2) . dilutional hyponatremia -> leads to fits/coma
183
describe 3 tests for SIADH and what they'd show
U&E
- dilutional hyponatraemia (low Na)
Osmolality
- low plasma osmolality
Urinalysis
- Urinary Na secretion
184
outline 4 management strategies for SIADH
1) . treat underlying cause
2) . restrict fluid (increases Na+ conc)
3) . DEMECLOCYCLINE
- inhibit ADH action on kidneys
- causes Diabetes insipidus
4) . TOLVAPTAN
- vasopressin receptor antagonist
- V2 blocker
185
define DIABETES INSIPIDUS
*lack of ADH*
```
Neurogenic = hyposecretion
Nephrogenic = insensitivity
```
186
list 5 Neurogenic causes of DIABETES INSIPIDUS
NEUROGENIC
1) . idiopathic
2) . tumour
3) . neurosurgery
4) . ADH gene mutation
5) . infection (TB)
187
list 5 Nephrogenic causes of DIABETES INSIPIDUS
NEPHROGENIC
1) . chronic renal disease
2) . drugs (lithium)
3) . hypercalcemia
4) . hypokalemia
5) . ADH receptor mutation
188
Outline the pathology of NEUROGENIC DIABETES INSIPIDUS
1) . disease of hypothalamus -> insufficient ADH made
| 2) . damage to post pituitary doesn't affect it as ADH can still leak out
189
Outline the pathology of NEPHROGENIC DIABETES INSIPIDUS
1) . channel disruption
| 2) . kidney damage -> doesn't respond to ADH
190
list 5 signs/symptoms of DIABETES INSIPIDUS
1) . polydipsia
2) . polyuria
3) . dehydration
4) . hypernatremia
5) . nocturia
191
list 4 investigations and what you would see for - Nephrogenic = osmolarity still low after adding DESMOPRESSIN (ADH analogue)
- Neurogenic = back to normal with DESMOPRESSIN
WATER DEPRIVATION TEST
- urine osmolarity low (diluted) after fluid restricted
MRI HYPOTHALAMUS
- confirms DI
URINE VOLUME
- high urine volumes confirm plyuria
U&E
- rule out more common issue
192
Changes to Water Deprivation Test to differentiate btwn neuro/nephrogenic DIABETES INSIPIDUS
Nephrogenic = osmolarity still low after adding DESMOPRESSIN (ADH analogue)
- Neurogenic = back to normal with DESMOPRESSIN
193
management for NEUROGENIC DIABETES INSIPIDUS
ADH analogue
| - Desmopressin
194
2 managements for NEPHROGENIC DIABETES INSIPIDUS
1) . Thiazide diuretics
| 2) . NSAIDs
195
Give example of 2 thiazide diuretics and how they works
1) .Bendroflumethiazide
2) .Hydrochlorothiazide
- increased Na+ secretion in DCT -> increased water loss -> body reduces GFR
196
how do NSAIDs work in treating NEPHROGENIC DIABETES INSIPIDUS
- inhibit prostaglandin synthase -> less prostaglandins -> reduced local ADH inhibition
197
Explain how the Parathyroid gland controls Calcium balance
*releases PTH -> more calcium*
1) . stimulates kidneys / GI tract to absorb more calcium
2) . stimulates osteoclasts to break down bones and released stored calcium
3) . increases Calcitriol levels (active Vit D) which increases GI/Kidney absorption of calcium
198
Explain how the Thyroid gland controls Calcium balance
*releases CALCITONIN -> less calcium*
1) . thyroid receptors stimulated when calcium gets too high
2) . this causes release of calcitonin
3) . calcitonin inhibits GI resorption
4) . calcitonin increases osteoblast activity
199
define HYPOCALCAEMIA
low serum calcium
200
list 5 causes of HYPOCALCEMIA
1). Actual Vit D deficiency (diet/sunlight/malabsorption)
2). Functional Vit D deficiency
(renal = no 1-hydroxylation)
(liver = no 25-hydroxylation)
3). Hypoparathyroidism
4). osteomalacia
5). Chronic Kidney Disease
201
outline the pathology of HYPOCALCAEMIA
CKD
1) poor renal calcium uptake
2) due to low active vit D production + renal phosphate retention
3) microprecipitation of calcium phosphate in tissues
202
5 symptoms of HYPOCALCAEMIA
1) . Spasms (Hands/feet/larynx/uterus)
2) . peripheral paraesthesia
3) . anxious
4) . seizures
5) . muscle tone UP
203
list 4 signs of HYPOCALCAEMIA
1) . convulsion
2) . arrhythmia
3) Chvostek's sign
4) . Trousseau's sign
204
what is Chvostek's sign
- tap over facial nerve where parotid gland is
| - causes twitching of ipsilateral facial muscles
205
what is Trousseau's sign
- carpopedal spasm (hands/feet)
| - induced by inflating BP cuff 20mmHg > systolic BP
206
outline the SPASMODIC mnemonic for signs / symptoms of HYPOCALCAEMIA
```
Spasms (Trousseaus)
Paraesthesia
Anxious
Seizure
Muscle tone up
Orientation impaired
Dermatitis (eczema)
Impetigo
Chvostek's sign
```
207
list 3 investigations and what you would see for HYPOCALCAEMIA
ECG
- long QT
FBC
- PTH high
eGFR
- search for CKD
208
treatment for mild HYPOCALCAEMIA
Adcal supplement
209
treatment for severe HYPOCALCAEMIA
calcium gluconate
210
define HYPERCALCAEMIA
high serum calcium
211
2 causes of HYPERCALCAEMIA
1) . primary hyperparathyroidism
| 2) . malignancy
212
outline the pathology of HYPERCALCAEMIA
*ectopic secretion of PTH is rare*
MALIGNANCY
- works by secreting PTH like peptide
- directly invades bone and produces local factors to mobilise calcium (unregulated bone breakdown)
213
list 10 symptoms of HYPERCALCAEMIA (Bones/Stones/Moans/Groans)
BONES
1) . painful bone condition
- osteitis fibrosa cystica
STONES
2). Ca deposition in renal tubules -> polyuria / nocturia. can lead to CKD
MOANS (Psych issues)
3) . lethargy
4) . depression
5) . psychosis
6) . memory loss
7) . fatigue
GROANS
8) . abdo pain
9) . nausea
10) . constipation
214
2 signs of HYPERCALCAEMIA
1) . polyuria
| 2) . polydipsia
215
2 investigations for HYPERCALCAEMIA
ECG
- short QT
FBC
- raised calcium
216
outline 3 treatments for HYPERCALCAEMIA
1) . loop diuretics -> return calcium to normal
2) . if primary hyperparathyroidism -> surgical removal of parathyroid adenoma
3) . IV bisphosphonates -> make osteoclasts apoptose to reduce bone resorption
217
define HYPERPARATHYROIDISM
excess PTH secretion
218
list 2 causes for PRIMARY HYPERPARATHYROIDISM
1) . single parathyroid adenoma
| 2) . hyperplasia
219
outline the pathology of PRIMARY HYPERPARATHYROIDISM
- adenoma / hyperplasia provides extra secretive tissue
| - excess PTH made
220
list the symptoms for HYPERPARATHYROIDISM (4 categories!)
*same as hypercalcemic*
BONES
- pain
STONES
- renal/biliary stones
ABDO GROANS
- nausea
- vomiting
- constipation
- indigestion
PSYCH MOANS
- fatigue
- depression
- psychosis
- memory loss
- lethargy
221
list 3 investigations for HYPERPARATHYROIDISM
1) . FBC
2) . DEXA bone scan for osteoporosis
3) . Abdo X-RAY for renal calculi
222
what blood results would you see in PRIMARY HYPERPARATHYROIDISM
- Ca high
- PTH high
- phosphate low
223
list 4 signs for HYPERPARATHYROIDISM
1) . fractures
2) . pain
3) . osteoporosis
4) . hypertension
224
management for PRIMARY HYPERPARATHYROIDISM
1) . if adenoma - surgical removal
2) . if hyperplasia - remove all 4 glands
3) . Calcimimetic (cinacalcet)
225
give example of calcimimetic and how it works
CINACALCET
- increase parathyroid cell sensitivity to Ca2+
- so less PTH secreted
226
list 3 causes of SECONDARY HYPERTHYROIDISM
1) . CKD
2) . low vit D
3) . malabsorption (any hypocalcemic disease)
227
outline pathology of SECONDARY HYPERTHYROIDISM
parathyroid gland becomes hyperplastic to compensate for chronic hypocalcemia
228
what would you see in bloods for SECONDARY HYPERTHYROIDISM
- Ca low
- PTH high
- phosphate high
229
management of SECONDARY HYPERTHYROIDISM
- treat underlying cause
230
cause of TERTIARY HYPERTHYROIDISM
develops from secondary hypoparathyroidism (CKD)
231
explain the pathology of TERTIARY HYPERTHYROIDISM
- glands become autonomous
| - produce excess PTH even when calcium deficiency corrected
232
what would you see in bloods for TERTIARY HYPERTHYROIDISM
- Ca high
- PTH high
- phosphate high
233
list 2 managements for TERTIARY HYPERTHYROIDISM
1) . calcium mimetic (cincalcet)
| 2) . parathyroidectomy
234
complication of PRIMARY HYPERTHYROIDISM if not treated
hypercalcemia
235
complication of SECONDARY HYPERTHYROIDISM if not treated
develops into tertiary hyperparathyroidism
236
complication of parathyroidectomy
transient hypocalcaemia
237
define HYPOPARATHYROIDISM
low levels of PTH
238
list 4 causes of HYPOPARATHYROIDISM
1) . could be transient
2) . common after anterior neck surgery
3) . genetic -> PTH gene defect
4) . autoimmune (Di-George)
239
outline the pathology of HYPOPARATHYROIDISM
1) . PTH normally stimulates vit D activation
2) . low PTH present means vit D functions don't occur
3) . result is hypocalcemia / hyperphosphatemia
240
list 4 functions of activated Vit D
- GI calcium absorption
- renal calcium absorption
- calcium release from bone
- inhibit phosphate reabsorption
241
list 6 symptoms of HYPOPARATHYROIDISM
*same as hypocalcaemia*
1) . increased excitability of muscles/nerves
2) . mouth/extremity paresthesia
3) . cramps
4) . convulsions
5) . tetany
6) . increased reflexes
242
2 signs for HYPOPARATHYROIDISM
*same as hypocalcemia*
1) . Chvostek's (twitching facial muscles over)
2) . Trousseau's (cardopedal spasm)
243
2 investigations for HYPOPARATHYROIDISM and the results
FBC
- Ca low
- PTH low
- phosphate high
ECG
- long QT
- HR / conctractility down
244
treatment for acute and persistent HYPOPARATHYROIDISM
ACUTE
- IV calcium
PERSISTENT
- Vit D analogue (alfacalcidol)
245
complication of treating HYPOPARATHYROIDISM
- could over treat with vit D
| - leads to hypercalcemia
