Endo Flashcards
1
Q
How does the pancreas know when to release insulin?
A
Amount of glucose that binds to GLUT-2 receptor on beta cells of pancreas
2
Q
How does indsulin cause the uptake of glucose into cells
A
Binds to insulin receptors which activate intracellular tyrosine kinase cascade. This results in increased expression of GLUT-4 channels on cell surface membrane.
3
Q
Where is thyroxine-binding globulin produced
A
Liver
4
Q
How does somatostatin affect hormones produced by antiterror pituitary
A
Inhibits Growth Hormone
5
Q
How does dopamine affect hormones produced in anterior pituitary
A
Inhibits prolactin
6
Q
Oxytocin and Vasopressin, which is paraventricular and which is supraorbital nucleas
A
Oxytocin in paraventricular and vasopressin is supraorbital
7
Q
What are the functions of cortisol?
A
Increases protein and carb breakdown, increases alpha 1 receptors on arterioles to increase BP, Suppresses immune response, increases osteoclast activity, increases insulin resistance
8
Q
What is MODY
A
Maturity-onset diabetes in young. Autosomal dominant mutation.
9
Q
What is the treatment for Mody
A
Sulfonylurea
10
Q
What is LADA
A
Latent autoimmune diabetes in adults
11
Q
What are the susceptible genes in T1DM
A
HLA DR2, HLA DR4DQ8
12
Q
Range for diabetes on random test
A
> 11.1 mmol/L
13
Q
How long do you fast before a fasting glucose test and what level do you expect to see in a diabetic
A
> 7mmol/L. 8 hours
14
Q
What is the treatment for T1DM
A
Basal Bolus Insulin
Basal:- Longer-acting to maintain stable insulin throughout the day
Bolus:- faster acting
15
Q
How would you describe the breathing of someone in DKA
A
Kussmal breathing (deep labored breaths to blow of CO2, compensation)
16
Q
What is first-line treatment for DKA
A
Always fluid then insulin (glucose and potassium as well)
17
Q
What has a greater genetic link, T1DM or T2DM
A
T2DM
18
Q
What is spinal level of thyroid
A
c5-t1
19
Q
What is the blood supply to the thyroid
A
Inferior thyroid artery, off thyrocervical trunk (subclavian)
Superior thyroid artery, off external carotid artery
20
Q
What do the follicular cells of the thyroid do
A
Trap iodine from circulation
21
Q
What is colloid
A
Fluid in thyroid that synthesis T3 and T4. Also producws thyroglobulin.
22
Q
What is the most common cause of hyperthyroidism
A
Graves
23
Q
Other than graves what can cause hyperthyroidism
A
Toxic multinodular goitre (nodules secrete thyroid hormones)
Toxic adenoma
Ectopic TSH secretion
24
Q
What hypersensitivity type is T1DM
A
Type 4
25
Diagnostic levels for DKA Ketones, Glucose
pH and HCO3-
Blood ketones:- >3mmol/l
Glucose:- >11.1mmol/L
pH:- ,7.3pH
HCO3-:- <15mmol
26
What is acanthosis nigracans
A skin pigmentation problem characterised by dark, velvety, and thick patches of skin usually formed in the skin folds and creases
27
What class of drug is metformin
Biguanide
28
What class of medication is gliclazide
Sulfonylureas. Stimulate more insulin release
29
How does the DPP-4 enzyme increase blood sugar levels
It inhibits GLP-1 (an incretin). GLP-1 stimulates pancreases to release more insulin and less glucagon, decreases gastric emptying and decreases appetite
30
What is the suffix for SGLT-2 inhibitors
Gliflozin
(Dapagliflozin, Canagliflozin, Empaglifozin)
31
What is the mechanism of action for SGLT-2 inhibitors
Inhibits the Sodium-Glucose Linked Transporter (SGLT) on the luminal side of the cells lining the proximal convoluted tubule leading to more glucose being excreted in the urine
32
What are the side effects of SGLT-2 inhibitors?
Risk of UTI (sugar in urine great environment for bugs), Thrush (candida infection), Weight loss (glucose pulls water into nephrons), low BP, dehydration, DKA with only moderately raised Blood Glucose
33
Macrovascular Complications of Diabetes Mellitus
Cardiovascualr (MI), Cebrovasular (stroke), PVD
34
Microvascular Complications of Diabetes Mellitus
Retinopathy, neuropathy (Charcot's foot), nephropathy (nephrotic syndrome CKD)
35
What is the treatment for hypoglycemia if no IV access
IM glucagon
36
Pathology of Graves disease
An autoimmune condition in which TSH receptor antibodies stimulate TSH receptors on the thyroid.
37
What is exophthalmos (proptosis)
Bulging of the eyeballs due to inflammation, swelling and hypertrophy of the tissue behind the eyes. Caused by TSH receptor antibodies in graves
38
What is pretibial myxoedema
Skin condition caused by deposits of glycosaminoglycans under the skin. Gives the skin a waxy, oedematous appearance and is specific to graves disease.
39
What are specific features to graves compared to other hyperthyrodism
Diffuse goitre without nodules
Graves eye disease, including exophthalmos
Pretibial myxoedema
Thyroid acropachy (hand swelling and finger clubbing)
40
Primary vs secondary TFT's in hyperthyrodism
Primary:- Low TSH High T4
Secondary:- High TSH High T4
41
How to differentiate between graves and TMG
Thyroid ultrasound
42
1st line treatment for hyperthyroidism
Carbimazole
43
What if Carbimazole is contraindicated in hyperthyroidism such as being pregnant
Propylthiouracil
44
What is a side effect of carbimazole
Agranulocytosis:- presents as a sore throat
45
Other than carbimazole, what is a treatment for hyperthyroidism
Radioactive Iodine (contraindicated in pregnancy)
Last resort:- surgery
46
What is a thyroid storm and what is the treatment
Rare presentation of hyperthyroidism with fever, tachycardia and delirium. Propylthiouracil and potassium iodide
47
What is the most common cause of hypothyroidism in developed world
Hashimotos thyroiditis
48
What is the most common cause of hypothyroidism in the developing world
Iodine definitely
49
What is the pathophysiology of hashimotos thyroiditis
Anti TPO antibodies attack thyroid
50
What are the symptoms of hypothyroidism
Cold intolerance, constipation, weight gain lethargy, menorrhagia
51
What are the signs of hypothyroidism?
Bradycardia, slow reflexes, cold hands, goitre
52
What will the TFT's show in primary vs secondary hypothyroidism
Primary:- High TSH, Low t4
Secondary:- Low TSH, low t4
53
What is the treatment for hypothyroidism
Levothyroxine (t4), titrate up dose to avoid hyperthyrodism
54
What is a complication of hypothyroidism
Myxedema coma:- usually infection precipitated. hypothermia and heart failure. Treat with levothyroxine and antibiotics + hydrocortisone until adrenal insufficiency is ruled out.
55
What are the types of thyroid carcinoma (and most common)
Papillary (most common), Follicular (25%), Anaplastic (Worst prognosis, metastasis the most)
56
How do the thyroid nodules in thyroid carcinoma present?
Hard and irregular
57
Gold standard investigation for thyroid carcinoma
Fine needle biopsy
58
Treatment for papillary and follicular thyroid carcinoma
Thyroidectomy or radioactive
59
What are the sites anaplastic thyroid carcinoma can metastasise to
Lung 50%, bone 30%, liver 10%, brain 5%
60
What is pseudo-Cushings
Caused by alcohol usually resolves in 1-3 weeks
61
The most common cause of Cushing's syndrome
Iatrogenesis (steroid use)
62
The most common cause of ACTH-dependent Cushings syndrome
Cushing's disease (pituitary adenoma)
63
Is CRH released more in the morning or night
Morning
64
Symptoms/ signs of Cushing's syndrome
Moon face, central obesity, purple abdominal striae, osteoporosis, thin peripheries, easy bruising, plethoric complexion, susceptible to infections, muscle atrophy.
65
1st line test for Cushing's
Random serum cortisol and if raised measure at 12 am (usually lowest point)
66
Explain Dexamethasone suppression test
Give a low dose, (1mg) should suppress
Then give a high dose 8mg, will supress adenoma but not ectopic ACTH
67
Treatment for Cushings disease
Transsphenoidal resection
or
Bilateral Adrenalectomy
68
What is a complication of a bilateral adrenalectomy
Nelsons syndrome, the Pituitary tumour will continue to enlarge with no negative feedback from adrenals. Massively increased ACTH and skin hyperpigmentation
69
What is the main cause of primary adrenal insufficiency in the developed world
Autoantibody-mediated adrenal destruction (Addisons)
70
What is the main cause of primary adrenal insufficiency in the developing world
TB + sarcoidosis
71
What is the most common cause of secondary adrenal insufficiency
Iatrogenic (suppression of hpa axis)
72
What is Waterhouse Fredrickson syndrome
Adrenal insufficiency due to adrenal haemorrhage. Most commonly due to meningococcal meningitis.
73
Why does Addisons cause hyperpigmentation
Excessive ACTH stimulates melanocytes
74
Do you get hyperpigmentation in secondary adrenal insufficiency
No, there is reduced ACTH
75
What are the signs/ symptoms are adrenal insufficiency
Lethargy, weight loss, postural hypertension( low aldosterone), Virtigo and change in body hair( reduced androgens) Hyperpigmentation in primary, Hypoglycemia, Abdo pain and vomiting
76
Gold standard test for adrenal insufficiency
Short Synthetic ACTH test, measure base cortisol at 9am when should be highest.
Then administer SYNACTH and if plasma cortisol raises after 30 mins exclude addisons
77
Primary vs Secondary Adrenal Insufficiency morning acth levels
Raised in primary
Low in secondary
78
What antibodies are present in Autoimmune addisons
21-hydroxy antibodies
79
Treatment for Adrenal Insufficiency
Hydrocortisone
80
What is excess HGH known as in children vs adults
Acromegaly in adults (after epiphyseal fusion)
Gigantism in children (before epiphyseal fusion)
81
What stimulates growth in infants
Nutrition and Insulin
82
What stimulates growth in children 3-11
Growth Hormone and Thyroxine
83
What stimulates growth in puberty
Growth hormone and sex steroids
84
What is growth Hormone also known as
Somatotropin
85
What factors can stimulate more growth hormone
Low blood glucose
Lack of food
Increased exercise
Increased sleep
Increased stress (trauma)
86
What is the network of capillaries known as that links the hypothalamus to the anterior pituitary
Hypophyseal portal system
87
How does GHRH cause the release of Growth hormone
Binds to a surface protein on somatotroph cells
88
What happens when GH reaches the liver, bones and muscles
They release somatomedins:- a small protein hormone that signals the anterior pituitary to stop producing growth Hormone
89
How do GH and somatomedins lead to less GH being produced
Cause hypothalamus to produce somatostain
90
Why do you have thick bones in acromegaly
GH stimulates osteoblast activity
91
What is the diabetogenic effect of GH
Increases insulin resistnace
92
What is the main cause of acromegaly
Pituitary adenoma (tumour of somatotrophs)
93
What are the signs/ symptoms of acromegaly
Large hands/ feet, box jaw, vision change, sleep apnoea (increase in larynx soft tissue), large interdental gaps, carpal tunnel syndrome, impaired glucose tolerance (risk of T2DM), joint/ back pain
94
What is the first line investigation for someone with acromegaly
IGF-1 serum level
95
What other endocrine disorder can acromegaly be associated with
Multiple Endocrine neoplasia type 1(Werner syndrome) affects parathyroid, pancreas and pituitary
96
What is the GS test for acromegaly
Impaired glucose tolerance, give high level of glucose:- should lower GH
97
What is the first-line treatment for acromegaly
Transsphenoidal surgery
Somatostatin analogues (octreotide)
GH receptor antagonists (pegvisomant)
Dopamine agonist (bromocriptine)
98
What are the complications of acromegaly
Carpal tunnel syndrome
T2DM
Congestive heart failure
Gastrointestinal Cancers (colon polyps)
99
Where is IGF-1 produced
Liver
100
What cells produce prolactin
Lactotroph cells of the anterior pituitary
101
Is hyperprolactinemia more common in males or females
Females
102
What is the main cause of hyperprolactinemia
Prolactinoma, (drugs like ecstasy can also cause this)
103
What are the symptoms of hyperprolactinemia
Amenorrhoea, Galactorrhoea + sexual disfunction, decreased libido, gynecomastia + decreased testosterone, bitemporal hemianopia
104
What is the test for hyperprolactinemia
Serum prolactin
105
What is the treatment for hyperprolactinemia
Dopamine agonists (cabergoline, bromocriptine):- massively shrinks tumour as dopamine inhibitor of prolactin.
106
What is Conn's syndrome
Hyperaldosteronism
107
What causes secondary hyperaldosteronism
Excess renin (usually suppressed in primary)
108
What is the most common cause of secondary hypertension
Conn's syndrome
109
What are the 2 main causes of Hyperaldosteronism
Adrenal adenoma (Conns) 66%
Bilateral adrenal hyperplasia 33%
110
What electrolyte changes are there in Conns syndrome
High sodium
Low potassium
111
Signs of conns syndrome
Resistant hypertension (unfixable with ACEi/ Beta blocker), Hypokalemia, muscle weakness, paresthesia, polydipsia + polyuria
112
What is the first line investigation for conns syndrome
Aldosterone: Renin ration is very high
113
What is the gold standard test for Conns syndrome
High serum aldosterone is not suppressed with o.9% IV saline or fludrocortisone.
(Also hypokalemia ECG findngs:- ST sagging, T wave depression, long PR)
114
Treatment for conns syndrome
Laparoscopic adrenalectomy Use spironolactone (aldosterone antagonist) 4 weeks pre-op.
115
How would you treat bilateral adrenal hyperplasia
Spironolactone (aldosterone antagonist)
116
Which cells of the collecting ducts does vasopressin affect
Principal cells (in CD and DCT) increase AQP2 channels on the apical membrane.
117
How many litres of dilute urine does someone urinate in diabetes insipidus
3L+
118
Causes of cranial DI
ADH gene mutation, pituitary adenoma
119
Causes of nephrogenic DI
Renal tubular acidosis, ADH receptor mutation, Hypercalcaemia, Hypokalaemia
120
Signs/ symptoms of Diabetes Insipidus
Polyuria, Polydipsia, Hypernatremia, lethargy confusion coma, severe dehydration
121
What is the investigation for Diabetes Insipidus
First:- Water deprivation test (8hr), normal- serum osm stays same and urine osm increases. Reveresed in DI
122
How to distinguish between Cranial and Nephrogenic DI
IM Desmopressin. In cranial DI Urine osm will be high but in nephrogenic will remain low.
123
Treatment for cranial DI
Desmopressin
124
Treatment for Nephrogenic DI
Thiazides (and treat underlying cause)
Thiazides increase sodium retention
125
SIADH is an overdiagnosed cause of ........
Hyponatremia (more water retention so NA+ excretion to compensate)
126
What tumour has the greatest link to SIADH
Small Cell Lung Cancer
127
What are the causes of SIADH
S:- SCLC
I:- Infection (TB)
A:- Abscesses
D:- Drugs (Sulfonylurea, SSRI, Carbamazepine)
H:- Head Trauma
128
Are AQP2 channels expressed more or less in SIADH
More to try an compensate:- leads to more Na+ loss
129
What are the symptoms of SIADH
Same as hyponatremia
Vomiting, Headache, decreased GCS (neurological deterioration), muscle weakness
Very severe:- seizures, brainstem herniation
130
Na+ and K+ serum levels in SIASH
Low Na+ and normal K+
131
Is urine osm high or low in SIADH
High. Dilute serum
132
How to distinguish between SIADH and a different cause of hyponatremia
Give 0.9% saline. Na+ depletion serum will normalise
SIADH:- serum fails to normalise
133
Treatment for SIADH (Acute)
Restrict fluid intake + hypertonic saline to concentrate blood
Treat underlying cause
134
Treatment for chronic SIADH
Furosemide, Vasopressin antagonist (tolvaptan), demeclocycline (for bacterial infections)
135
What is a carcinoid tumour
A tumour of neuroendocrine cells (enterochromaffin cells in GI or in lungs)
136
What is carcinoid syndrome?
The group of symptoms associated with a carcinoid tumour (when it metastasises to the liver) secrete 5-HT/ serotonin
137
, What is the most common site for a carcinoid tumour
GIT @ Appendix+ terminal ilium
138
What are the symptoms of carcinoid syndrome
Flushing, diarrhoea, tricuspid incompetence (valve lesion), resp problems
139
How to diagnose Carcinoid syndrome
Liver US, Increase in 5hydroxyudleactic acid (main metabolite of serotonin) in urine GS
140
What is the definitive treatment of carcinoid syndrome
Surgically excise primary tumour
141
What is the pharmacological treatment for carcinoid syndrome
Octreotide (somatostatin analogue) can block tumour hormones
142
What is a complication of a carcinoid crisis and what is the treatment
Life-threatening carcinoid syndrome symptom constellation
Treat with high dose octreotide
143
What is a phaeochromocytoma
An adrenal medullary tumour (of the chromaffin cells) secretes catecholamines (NAd, Adr)
Is a secondary cause of hypertension
144
What is the cause of a phaeochromocytoma
Usually inherited, associated with multiple endocrine neoplasia 2A+ 2B
Neurofibromatosis 1 (Tumours deposited along myelin sheath)
145
Symptoms of phaeochromocytoma
Hypertension, pallor, very sweaty, tachycardic
146
How would you diagnose phaeochromocytoma
Plasma metanephrines (longer half-life than NAd/ Adr) + normetanephrine (metabolite of NAd)
147
What is the treatment for phaeochromocytoma
Alpha blockers (phenoxybenzamine)
then Beta blockers after to prevent reactive vasoconstriction
If surgery possible excise tumour
148
Is parathyroid hormone released when Ca+ is high or low
Low
149
What cells of the Parathyroid releases PTH
Cheif cells
150
How does PTH stimulate osteoclast activity
Inhibits OPG which competes with RANK-L
151
How does PTH affect the kidneys
Increases calcium reabsorption in Ascending loop of Henle, DCT and CD.
Decreases phosphate reabsoprtion
152
How does PTH cause an increase in calcium absorption in the small intestine
Activates calcitriol (active vitamin D) (1,25-dihydroxycholecalciferol)
153
What % of hypercalcemia is due to hyper parathyroid in the community
90%
154
What is the most common cause of hypercalcemia in hospitals
Bone malignancies (myeloma)
155
What is the most common cause of HypoPTH
CKD
156
What is the most common cause of hyperPTH
Primary:- Parathyroid adenoma (sometimes parathyroid hyperplasia)
157
What is secondary Hyperparathyroidism
Physiological response to low Ca+ (in CKD + Vit D deficiency)
158
What is tertiary hyperPTH
After many years of secondary, glands act autonomously with no negative feedback.
159
How do cancers such as squamous cell lung, breast and renal cancer cause hyperparathyroidism
Secrete Parathyroid related protein
160
What are the symptoms of HyperPTH
Hypercalcemia
Bones (osteopenia)
Stones (kidney stones)
Groans (abdo pain + constipation)
Psychedelic moans ( depression, anxiety)
Short QT on ECG
161
What is the treatment for primary hyperPTH
Remove parathyroid glands
162
What is the treatment for acute severe hypercalcemia
Give IV fluids + bisphosphonates
163
What is a primary cause of HypoPTH
DiGeorge syndrome (a small part of chromosome 22 is missing), pth glands don't develop (rare)
164
What is secondary hypoPTH
Post parathyroid/thyroidectomy
More common than primary
165
What is pseudohypoPTH, and what are the symptoms
Peripheral resistance to PTH
Short stature+ small 4th/5th metacarpals
166
What are the symptoms of HypoPTH
Hypocalcemia
CATS go numb
C:- Convulsions
A:- arrhythmia
T:- tetany (involuntary contractions of muscles)
Numbness
167
What are the 2 signs of HypoPTH/ hypocalcemia
Chovestek:- twitching of facial muscles when CN7 tapped just in front of ears
Trousseau:- carpopedal spasm when applying tourniquet to forearm
168
What is the treatment for hypoPTH
Calcium supplements + vit D3
169
Is muscle tone increased or decreased in hypercalcemia
Decreased:- Ca+ inhibits Na+ influx
170
Why does CKD cause hypocalcemia
Reduced vitamin D activation
171
Does acute pancreatitis cause hyper or hypocalcemia
Hypocalcemia
172
Causes of hyperkalaemia
AKI
Spironolactone
Addison's
DKA
173
Why does hyperkalemia lead to abnormal heart rhythms
K+ decreases threshold action potential due to easier depolarisation
174
ECG changers for hyperkalaemia
GO:- Absent P waves
Go long:- long PR
Go tall:- Tall tented T waves
Go wide:- Wide QRS
175
What is the treatment for hyperkalemia if urgent
Calcium Gluconate then insulin + dextrose
176
What does calcium gluconate do
Stabilizes cardiac cell wall membrane
177
Treatment for non-urgent hyperkalemia
Insulin + dextrose
178
How does insulin help in hyperkalemia?
Insulin stimulates the activity of Na+ H+ antiporter on the cell membrane promoting the entry of sodium into cells. This then causes Na+ K+ ATPase activation causing an influx of potassium
179
What are the causes of hypokalemia
Thiazides (Na+ sparring), loop diretics, Conn's, Renal Tublar acidosis, GI losses
180
What are the symptoms of hypokalemia
Hypotonia, hyporeflexia, arrhythmia (especially af)
181
ECG changes in hypokalemia
Small inverted T waves, Prominent U waves, St depression, PR prolongation
