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Mattias - Endocrine > Deck 4 > Flashcards

Deck 4 Flashcards

1
Q

Where is ADH and Oxytocin synthesized

A

Hypothatlmus

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2
Q

Where is ACTH, LH, TSH and FSH synthesized

A

In the anterior pituitary

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3
Q

Causes of anterior pituitary hyperfunction

A

Adenoma or Carcinoma

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4
Q

Causes of anterior pituitary hypofunction

A 
Surgery/Radiation
Sudden hemorrhage into gland
Ischemic necrosis (Sheehan Syndrome)
Tumors extending into sells
Inflammatory conditions (Sarcoidosis)
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5
Q

Causes of Syndrome of Inappropriate ADH secretion (SIADH)

A

Extopic ADH secretion by tumors

Primary disorder in the pituitary

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6
Q

How are pituitary adenomas classified

A

By cell type/hormon produced

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7
Q

What condition is Pituitary adenoma related to

A

Multiple Endocrine Neoplasia Type 1 (MEN1)

Werner’s syndrome

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8
Q

What may happen with large pituitary adenomas

A

Visual field defects
Pressure atrophy
Infarction can lead to panhypopituitarism

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9
Q

Most common functional Pituitary adenoma

A

Prolactinoma (30%)

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10
Q

Signs of prolactinoma

A

Infertility
Lack of libido
Amenorrhea (25%)

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11
Q

Second most common functional pituitary adenoma

A

Growth hormone secreting tumor

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12
Q

Signs of Growth hormone secreting adenoma

A

Increased IGF-1
Growth of Bone,cartilage and connective tissue
Giantism or Acromegaly

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13
Q

Which functional pituitary adenoma causes Cushing’s syndrome

A

ACTH Secreting

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14
Q

Features of an ACTH secreting pituitary adenoma

A

Usually a microadenoma

Bilateral adreno hyperplasia

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15
Q

How common are pituitary carcinomas

A

Rare <1% of pituitary tumors

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16
Q

Features of pituitary hypofunction

A

Usually panhypopituitarism, rarely affect only one hormone

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17
Q

What brain tumor is derived from remnants of Rathke’s pouch

A

Craniopharyngioma

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18
Q

Where is Craniopharyngioma anatomically located

A

Some arise within the sella but most are suprasellar

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19
Q

When is Cranioharyngioma occuring, age wise

A

Bimodal incidene
5-15 years of age
6th-7th decade

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20
Q

Signs and sumptoms of Craniopharyngioma

A

Headaches and visual disturbance

Children may have growth retardation

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21
Q

Prognosis of Craniopharyngioma

A

Good prognosis, especially if ,5cm

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22
Q

Causes of Cranial Diabetes insipidious

A

Trauma
Surgery
Tumors and inflammatory disorders of hypothalmus and pituitary

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23
Q

How big are the adrenal glands

A

4.5 gram each

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24
Q

What are the two regions of the adrenal gland

A

Outer cortex and central medulla

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25
Q

What are the three zones of the Adrenal cortex from outer to inner

A

Zona glomerulosa
Zona Fasciculata
Zona Reticularis

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26
Q

What is produced in the Zona Glomerulosa

A

Mineralocorticoids - Aldosterone

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27
Q

What is produced in the Zona Fasciculata

A

Glucocorticoids - Cortisol

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28
Q

What is produced in the zona Reticularis

A

Sex steroids + Glucocorticoids

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29
Q

What is a catecholamine

A

Organic compound that has a benzene ring with two hydroxylgroups and a side amine

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30
Q

Examples of Catecholamines

A

Dopamine
Noradrenaline/Norepinephrine
Adrenaline/Epinephrine

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31
Q

Where are the catecholamines secreted from

A

Neuroendocrine (Chromaffin) cells in the adrenal medulla

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32
Q

What innervates the adrenal medulla (nerve type)

A

Pre-synaptic sympathetic neurones

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33
Q

Causes of hyperfunction of adrenal cortex

A

Hyperplasia
Adenoma
Carcinoma

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34
Q

Causes of hypofunction of the adrenal cortex

A

Acute - Waterhouse-Friderichsen

Chronic - Addison’s disease

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35
Q

What type of cancer often produce ectopic ACTH

A

Small cell lung carcinoma

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36
Q

What’s the backfround of Diffuse or Nodular adrenocortical hyperplasia

A

Diffuse is ACTH driven

Nodular is usually ACTH independent

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37
Q

Causes of Congential Adrenocortical hyperplasia

A

Autsomal recessive disorders, disrupted steroid synthesis leads to increased ACTH which causes Adrenal hyperplasia

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38
Q

What is the Waterhouse-Friderischen syndrome

A

Acute adrenal failure due to bleeding into adrenal glands caused by severe bacterial infection, most commonly the Meningococcus Neisseria meingitdis

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39
Q

Features of Adrenocortical adenomas

A

Small (2-3cm)
Well circumscribed, encapsulated lesions
Yellow-brown surface
Most likely non functional

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40
Q

Features of Adrenocortical carcinomas

A

Rare
More likely to be functional
Bad prognosis (5y survival 20-35%, 2y survival 50%)
Local or vascular spread

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41
Q

Suggestive features differing Adrenocortical carcinomas from adenomas

A

Meatstasis only feinite.
Large size (>50g or >20cm)
Hemorrhage, Necrosis, invasion, atypical mitoses

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42
Q

What is Conn’s syndrome

A

Primary hyperaldosteronism

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43
Q

Causes of secondary hyperaldosteronism

A

Increased Renin
Decreased Renal perfusion
Hypovolemia
Pregnancy

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44
Q

Causes of Primary hyperaldosteronism

A

60% associated with diffuse or nodular hyperplasia

35% Adenomas

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45
Q

What is Cushing’s syndrome

A

Hypercortisolism

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46
Q

What is Cushing’s disease

A

Specific type of Cushing’s syndrome caused by a pituitary tumor with increased ACTH secretion

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47
Q

Causes of hypercortisolism, main groups

A

Iatrogenic (steroid therapy/abuse)
ACTH dependent
ACTH independent

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48
Q

Causes of ACTH dependent hypercortisolism

A 
ACTH secreting pituitary adenoma (70%)
Ectopic ACTH (10%)
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49
Q

Causes of ACTH independent hypercortisolism

A 
Adrenal adenoma (10%)
Adrenal Carcinoma (5%)
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50
Q

Three common causes of Chronic primary Adrenocortical insufficiency

A

Autoimmune adrenalitis
Infections (TB, Fungal, HIV)
Metastatic malignancy

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51
Q

Causes of acute primary Adrenocorticol insufficency

A

Rapid withdrawal of steroid treatment
Excacerbation of chronic condition
Adrenal Hemorrhage (Waterhouse-Frerischen syndrome)

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52
Q

Symptoms of Addison’s Disease

A

Vague
Weakness, fatigue, Anorexia, Nausea, Vomiting, Weight loss, diarrhea
Pigmentation (Increased ACTH)

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53
Q

What causes pigmentation in Addison’s disease

A

Increased ACTH as a response to low cortisol levels

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54
Q

What is the onset of Addison’s crisis

A

Stress - infection, trauma, surgery

Anything that increases the body’s need for extra steroids

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55
Q

Results of decreased mineralocortocoids

A 
K+ retention
Na+ loss
Hyperkalemia
Hyponatremia
Hypotension
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56
Q

Results of decreased glucocorticoid

A

Hypoglycemia

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57
Q

Types of adrenal medullary tumors

A

Phaeochromocytoma

Neuroblastoma

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58
Q

What cells are Phaeochromocytoma derived from

A

Chromaffin cells of the adrenal medulla

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59
Q

What does Phaeochromocytoma tumors secrete

A

Catecholamines

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60
Q

Complications of Phaeochromocytoma

A

Cardiac failure
Infarction
Arrythmias
Cerebrovascular accident (CVA)

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61
Q

Laboratory diagnosis of Phaeochromocytoma

A

Detection of urinary excretion of Catecholamines and metabolites

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62
Q

90% of Phaeochromocytomas causes

A

Hypertension

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63
Q

What are extra adrenal Paheochromocytomas called

A

Paragangliomas

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64
Q

Why is Phaeochromocytoma called the 10% tumor

A

10% extra adrenal
10% bilateral
10% malignant
10% are NOT causing hypertension

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65
Q

Which Multiple Endocrine Neoplasia Type is Phaeochromocytoma associated with

A

MEN 2A

MEN 2B

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66
Q

What neoplasias are associated with MEN 2A

A

Phaeochromocytoma
Medullary thyroid carcinoma
Parathyroid hyperplasia

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67
Q

Which neoplasia is a feature of MEN 2B

A

Phaeochromocytoma
Medullary thyroid carcninoma
Neuromas and Ganglioneuromas
Marfanoid habitus

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68
Q

What are the anatomical boundaries of the anterior triangle

A

Superiorly - Mandible
Medially - Midline of body
Laterally - Anterior border of Sternocleidomastoid

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69
Q

What are the anatomical boundaries of the Posterior triangle

A

Anteriorally - Posterior border of the sternocleidomastoid
Laterally - Anterior border of Trapezius
Inferiorally - Clavicle

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70
Q

How to distinguish between goitre and thyroglossal duct cyst on examination

A

Thyroglossal duct cysts move with the tongue

Both move on swallowing

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71
Q

Lab rankings of suspected thyroid malignancy fine needle aspiration and treatment

A 
Thy 1-5.
Thy1 = Inadequate sample, repeat
Thy2 = Benign, repeat in 6 months
Thy3 = Suspicious, Thyroid lobectomy
Thy4 and Thy5 = Malignant, Total Thyroidectomy
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72
Q

What is cystic hygroma

A

Often congenital lympharic lesion classically in left posterior triangle.
Lymph filled cyst that transilluminate

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73
Q

What is a Branchial cyst

A 
Persisting second branchial arch
Upper part of Anteror triangle
Fells like a "Half filled hot water bottle"
FNA - Cholesterol crystals
May fistulate
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74
Q

What are the two types of bones and % distribution

A

Trabecular and Cortical
80% Cortical
20% Trabecular

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75
Q

What are the features of Trabecular bone

A

Porous, sponge like

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76
Q

What are the features of Cortical bone

A

Dense

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77
Q

What are the regulating factors of Peak Bone Mass

A 
Genetics (70-80%)
Body weight
Sex hormones
Diet
Exercise
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78
Q

What are the regulating factors of Bone Loss

A 
Sex hormone deficiency
Body weight
Genetics
Diet
Immobility
Diseases
Drugs (Glucocorticoids)
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79
Q

What changes are seen in the microarchitecture of bone in osteoperosis

A

Loss of bone

Thinning of trabeculae in all plaes leading to breakage

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80
Q

Risk factures for fracture

A 
Previous fragility fracture
Glucocorticoid usage
History of falls
FH of hip fractures
Other secondary causes of osteoperosis
Low BMI (10/day)
Alcohol intake (>4 units/day)
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81
Q

What is the risk of hip fracture with a previous Colles fracture

A

Double the risk of hip fracture

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82
Q

What endocrine condition is a secondary cause of osteoperosis

A

Hyperthyroidism
Hyperparathyroidism
Cushing’s disease
T1DM

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83
Q

GI condition that are secondary cause of Osteoperosis

A

Celiac
Inflammatory bowel disease (IBD)
Chronic liver disease
Chronic pancreatitis

84
Q

Direct effect on bone by corticosteroids

A

Decreased osteoblast activity and lifespan
Decreased Calcium absorption
Decreased replication of osteoblast precursors

85
Q

What does BMD stand for

A

Bone Mineral Density

86
Q

How do you investigate Bone Mineral Density (BMD)

A

DEXA scan

87
Q

What is the effect on BMD with glucocorticoid use

A

Rapid loss
30% in first 6 months
Partially reversible

88
Q

What is the T score comparing with in a DEXA scan

A

Young adult female population mean

89
Q

What is the Z score comparing with in a DEXA scan

A

Age-matched sex population mean

90
Q

What is a normal T-score in a DEXA scan

A

Bone Mineral Density within one standard deviation of the young adult reference mean
T-score<1 SD of mean

91
Q

What is the T-score in Osteopenia

A

BMD> 1 SD below mean

BMD<2.5 SD below the mean

92
Q

What is the T score in Osteoperosis

A

BMD >2.5 SD below the mean

BMD =2.5 SD below the mean

93
Q

When is the Z score used

A

Patients younger than 20

94
Q

Lifestyle management of osteoperosis

A

High intensity strength training
Low impact exercises
Avoidance of excess alcohol and smoking

95
Q

Diet management of osteoperosis

A

Reference Nutrient Intake of Calcium is 700mg

Post menopausal women aim at 1000mg of Calcium/day

96
Q

Food sources of Calcium

A

Milk and Dairy
Bread and fortified cereals
Fish with bones
Nuts, green vegatables and bean

97
Q

When should you treat with antiresorptive therapy

A

T score >2.5 below mean
On >7.5 mg Prednisolone/day for >3 months
Vertebral fracture + T score >1.5 below mean

98
Q

Examples of drugs to treat Osteoperosis

A 
Calcium and Vitamin D supplement
Bisphosphonate
Denosumab
Strontium Ranelate
Teriparatide
Hormone Replacement Therapy (HRT)
Testosterone
SERMS (Selective Estrogen Receptor Modulators)
99
Q

Who should take Calcium supplementation in tablet form

A

Post menopausal women unable to get 1000 mg Calcium from diet

100
Q

Who doesn’t need Vitamin D supplementation

A

People <65 years with adequate sun exposure

101
Q

Dosage of Vitamin D supplementation

A

10ug/day for >65y

20ug/day for frail elderly housbound women

102
Q

Examples of Bisphosphonates

A

Alendronate

Risedronate

103
Q

Mode of action of Bisphosphonates

A

Ingested by osteoclasts leading to apoptosis which inhibit bone resorption

104
Q

Effect on BMD by Bisphosphonates

A

Increase by 5-8%

105
Q

Long term concerns of Bisphosphonates

A

Osteonecrosis of jaw
Esophageal cancer
Atypical fractures

106
Q

What is the route of administration for Zoledronic acid and how often

A

Once yearly IV infusion

three years of therapy

107
Q

Dosage of Zoledronic acid

A

5mg in 100 mls NaCl over 15min

108
Q

Benefit of Zoledronic acid

A

About 70% reduction in vertebrae fractures

40% reduction in hip fractures

109
Q

What type of drug is Zoledronic acid

A

Bisphosphonate

110
Q

What is Denosumab

A

Fully human monoclonal Antibody used in Osteoperosis treatment

111
Q

Mode of action of Denosumab

A

Targets and binds with high affinity and specificity to RANKL (Receptor Activator of Nuclear Factor-kB ligand)
This blocks RANKL to bind on RANK which is present on pre-osteoclasts which inhibit osteoclast development

112
Q

Route of administration of Denosumab

A

Subcutaneous injection

6 monthly

113
Q

Adverse effects of Denosumab

A

Eczema

Cellulitis

114
Q

What are the contraindications of Strontium Ranelate

A

History of Thromboembolic disease, IHD, Peripheral arterial disease, Uncontrolled hypertension

115
Q

What line of treatment is Strontium Ranerlate in Osteoperosis

A

Third line

116
Q

Mode of action of Strontium Ranelate

A

Stimulate Calcium sensing receptros which increase osteoblast formation and reduce osteoclast formation from their precursors which increase bone mass and strength

117
Q

What is Teriparatide

A

Recombinant parathyroid hormone used in Osteoperosis treatment

118
Q

Mode of action of Teriparatide

A

As an analogues of PTH, intermittent exposure activates osteoblasts more than osteoclasts leading to a net bone growth

119
Q

Route of administration of Teriparatide

A

Daily Subcutaneous injections

120
Q

What sequence of PTH is Teriparatide

A

Amino acid 1-34 out of PTH’s 84

121
Q

How long is Teriparatide treatment and what is it taken with

A

18-24 months

Supplemented with Calcium and Vitamin D

122
Q

Negative about Teriparatide

A

Extremely expensive

3534 GBP/year vs Alendronate 14GBP/year

123
Q

Parathyroid hormone activate what bone cells causing what

A

Osteoclasts causing bone resorption and increased serum Calcium

124
Q

How is PTH release controlled

A

Increased Calcium binds to Calcium sensing receptor (CaSR) on the parathyroid gland inhibiting PTH release

125
Q

What is the effect of PTH on the GI tract

A

Increases Calcium absorption

126
Q

How is Vitamin D syntheized in the skin

A

Dehydrocholesterol –(+UVB rays)–> Cholecalciferol (D3) –(Converted in liver)–> 25-hydroxyl Vitamin D –(converted in Kidneys)–> 1,25-hydroxyl Vitamin D

127
Q

In what form is Vitamin D absorbed in the GI tract

A 
Vitamin D3 (Cholecalciferol)
Vitamin D2 (Ergocalciferol)
128
Q

What has to happen to Vitamin D3 (Cholecalciferol) to become active

A

Has to be hydroxylated in both the liver and the kidneys

129
Q

Menomonic for hypercalcemia

A

Stones, groans, bones and psychic moans

130
Q

In hypercalcemia mneomonic, what does stones refer to

A

Renal stones

131
Q

In hypercalcemia mneomonic, what does groans stand for

A

Abdominal symptoms

Constipation, indigestion, nausea, vomiting, pain, acute pancreatitis, ulcers

132
Q

In hypercalcemia mneomonic, what does bones stand for

A

Bone related complications
Osteopenia/Osteoperosis
Osteomalacia
Fractures

133
Q

In hypercalcemia mneomonic, what does Psychic moans stand for

A

CNS effect

Depression, lethargy, fatigue, memory loss

134
Q

What are symptoms of acute hypercalcemia

A

Thirst
Dehydration
Confusion
Polyuria

135
Q

Causes of hypercalcemia, most common

A

Primary hyperparathyroidism
Malignancy
Together account for 90% of hypercalcemia

136
Q

Diagnosis of Primary Hyperparathyroidism

A

Raised serum Calcium
Raised PTH or high normal
Increased urine Calcium exretion

137
Q

Why does malignancy sometimes cause hypercalcemia

A

Certain cancer cells secretes parathyroid hormone related proteins which act as PTH

138
Q

What malignancies are most commonly assoicated with hypercalcemia

A 
Squamous cell lung cancer
Breast
Squamous cell of head and Neck
Multiple Myeloma
Ovarian
139
Q

Diagnosis of hypercalcemia of Malignancy

A

Increased Calcium
Increased ALP
X-ray, MRI, CT and Isotope bone scan

140
Q

Treatment of Acute Hypercalcemia

A

Rehydration (0.9% saline 4-6L in 24h)
Avoid thiazide diuretics, use loop diuretics
Bisphosphonates

141
Q

Management of primary hyperparathyroidism

A

Surgery or nothing

142
Q

What is Osteitis Fibrosa cystica

A

Skeletal disorder caused by hyperparathyroidism which cause increased osteoclast activity and bone resorption, weakening and loss of bone which is replaced by fibrous tissue and formation of cyst-like tumors in and around the bones (Pepper pot skull sign)

143
Q

Indications for Parathyroidectomy

A

End organ Damage (Ulcers, stones, osteoperosis, Osteitis Fibrosa Cystica)
Serum Calcium >2.85 mmol/L
Under age 50
eGFR <60 ml/min

144
Q

Which multiple Endocrine Neoplasia is associated with hypercalcemia

A

MEN1

MEN2

145
Q

Cause of following blood sample results
Increased calcium
Increased albumin
Increased Urea

A

Dehydration

146
Q

Symptoms and signs of Hypocalcemia

A 
Paraesthesia of fingers and toes
Perioral muscle weakness
Cramps, Tetany, Fatigue, Fits
Bronchospasm or Laryngospasm
Chocesteks sign, Trousseau sign
QT Prolongation
147
Q

Waht is paraesthesia

A

Pines and needle sensation

148
Q

Describe Chovstek’s sign

A

Innapropriate hyperexcitability of facial nerve.
Tapping on the facial nerve at the angle of the jaw by the masseter causes twitching of face muscles occour on the same side. Seen as a nose or lip twitch

149
Q

Describe Trosseau sign

A

Inflate a BP cuff above systolic on the arm for three minutes.
If hypocalcemic, spasm will occur with wrist and MCP flexion and DIP,PIP extension

150
Q

Main causes of hypocalcemia

A

Hypoparathyroidism, Vitamin D deficiency, Chronic renal failure

151
Q

Treatment of acute hypocalcemia

A

IV Calcium gluconate, 10ml, 10% over 10 min

152
Q

Causes of hypoparathyroidism

A 
Congenital absence (DiGeorge Syndrome)
Destruction (surgery, radiotherapy, malignancy)
Autoimmune
Idiopathic
Hypomagnesemia
153
Q

Long term management of hypoparathyroidism

A

Calcium supplement 1-2g/day

Vitamin D supplement, tablet or injection

154
Q

What is Vitamin D tablets called

A

1-alpha calcidol

155
Q

What is pseudohypeparathyroidism

A

Genetic defect of G protein alpha subunit (GNAS1 gene) causing PTH resistance

156
Q

Signs and symptoms of pseudohypoparathyroidism

A

Low Serum Calcium
High PTH
Bone Abnormalities, obesity, subcutaneous calcification, mental retardation, Brachdactyly of the 4th metacarpal

157
Q

What is Brachdactyly

A

Shortness of the digits, both fingers and toes

158
Q

What is pseudopseudohypoparathyroidism

A

Same as pseudohypoparathyroidism but with normal Calcium levels

159
Q

What are the disorders caused by Vitamin D deficency called

A

Ricket’s in children

Osteomalacia in adults

160
Q

Causes of Rickets and Ostemalacia

A 
Dietary deficiency of Vitamin D
Malabsorption (gastric surgery, Celiac disease, liver disease, pancreatic failure
Chronic renal failure
Lack of sunlight exposure
Drugs (ex anticonvulsant)
161
Q

Clinical findings in Osteomalacia

A

Reduced Serum Calcium
Proximal myopathy and muscle waisting
Dental caries, enamel
Bone (tenderness, fracture, Rib and limb deformities)

162
Q

What are Looser Zones

A

Also called pseudofractures, seen in Osteomalacia. Common sites, scapula, pubic ramus, proximal femur medially

163
Q

How does Chronic renal disease cause hyperparathyroidism

A

Chronic renal failure causes Vitamin D deficiency because the kidney can’t convert 25-OH Vit D to 1,25-OH Vit D. This leads to secondary hyperparathyroidism with increased PTH and increased 25-OH Vit D

164
Q

What are the lab findings in extreme reduced sun exposure

A 
Reduced Calcium
Reduced Phosphate
Increased Alk Phosphate
Decreased 25-OH Vit D
Increased PTH
165
Q

What is Paget’s disease

A

Abnormality of bone remodeling, often only affect one or a few bones

166
Q

Signs symptoms and clinical findings in Paget’s disease

A

Often asymptomatic, bone pain, fractures, nerve compression (deafness) Increased Alk phosphate

167
Q

Management of Paget’s disease

A

High dose oral Bisphosphonates (2-6 months)

Subcutaneous injection of Calcitonin

168
Q

What is Vertebroplasty

A

Treatment for vertebral fractures that has not responded to conservative measures. Bone cement is injected into the vertebral body. Does not restore vertebral height

169
Q

Side effect of Thiazolidinediones

A

Liver impairment, weight gain, fluid retention

170
Q

What is the treatment for Addison’s disease

A

Hydrocortisone +Fludrocortisone

Replace both glucocorticoids and mineralocorticods

171
Q

What is the main effect of mineralocorticoid

A

Fluid retention

172
Q

What is ocogenesis

A

Creation of an egg (ovum)

173
Q

Two phases of the overias cycle are

A

Follicular phase and Luteal phase

174
Q

When in the ovarian cycle is ovulation

A

End of follicular phase

175
Q

When is the corpus luteum developed

A

In the luteal phase of the ovarian cycle

176
Q

What is FSH action in the ovary

A

Stimulate development of follicels

177
Q

What is LH action in the ovary

A

Stimulate follicle maturation, ovulation and corpus luteum develpment

178
Q

First line treatment of hypertension in Diabetics

A

ACE inhibitors regardless of age

179
Q

What drug increases the risk of edema in a patient taking Pioglitazone

A

Insulin

Pioglitazone is a Thiazolidinedione who’s side effect is fluid retention

180
Q

Most common Antibody in Hashimoto’s thyroiditis

A

Anti-thyroid peroxidase Antibody

181
Q

What is the best diagnostic test of Cushing’s syndrome

A

Overnight Dexamethasone suppression test

182
Q

Impaired fasting glucose is mainly due to

A

Hepatic insulin resistance

183
Q

Impaired glucose tolerance is mainly due to

A

Muscle insulin resistance

184
Q

Impaired fasting glucose is more likely to develop T2DM than Impaired glucose tolerance
True or False

A

False. IGT patients are more likely to develop T2DM

185
Q

What features are seen in Grave’s disease but not other hyperthyroid conditions

A

Exophthalmos
Ophthalmoplegia
Pretibial myxoedema
Thyroid Acropatchy

186
Q

What type of drug are -gliptins (ex Sitagliptin)

A

Dipetptidyl peptidase-4 (DPP-4) inhibitor

187
Q

At what rate should insulin be given IV in DKA

A

0.1 units/kg/hour

188
Q

What kind of drug i Dapagliflozin

A

SGLT-2 inhibitor

189
Q

What drugs can you combine with Exenatide

A

Exanatide should ONLY be used with Metformin, Sulfonylureas or both

190
Q

Inheritance pattern of MEN

A

Autosomal dominant pattern

191
Q

Urea and electrolyte blood results in Cushing’s syndrome

A

Hypokalemiaic metabolic alkalosis

192
Q

What is the relation between HbA1c and average plasma glucose

A

Average plasma glucose = (2*HbA1c)-4.5

193
Q

What kind of drug is Glimepiride

A

Sulfonylurea

194
Q

First line treatment of Neuropathic pain

A

Amitriptyline
Duloxetine
Gabapentin
Pregabalin

195
Q

Features of Primary hyperaldosteronism

A

Hypertension
Hypokaremia
Alkalosis

196
Q

Major adverse effects of Exenatide

A

Nause and vomiting

197
Q

Minimum HbA1c to diagnose T2DM

A

6.5% (48mmol/L)

198
Q

Symptoms of Gastroparesis in Diabetics

A

Erratic blood glucose control, bloating and vomiting

199
Q

Management of Gastroparesis in Diabetes

A

Prokinetic drugs =
Metocloppramide
Domperidone
Erythromycin

200
Q

What are prokinetic drugs

A

Drugs that enhance GI motility by increasing contractions in the small intestine

201
Q

What is Addison’s disease associated with, metabolic alkalosis or acidosis

A

Metabolic acidosis

202
Q

What anti-hypertensive combination should be avoided in Diabetics

A

Beta-blockers+Thiazide diuretics

May cause insulin resistance and change autonomic response to hypos

203
Q

Most common gene involved in MODY

A

HNF-1 alpha, MODY3 which is 60% cases

204
Q

What drug is good in diabetics with an erradic lifestyle

A

Meglitinides

205
Q

What diabetic drug is associated with severe pancreatitis and renal impairment

A

Exenatide

Mattias - Endocrine (4 decks)

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