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Clin Med 2 > Exam 5 > Flashcards

Exam 5 Flashcards

1
Q

C peptide

A

Will be high if they are insulin resistant, but low if they are insulin deficient (type 1)

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2
Q

Microvascular complications

A

Retinopathy
Nephropathy
Neuropathy

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3
Q

Macrovascular

A

Cardiovascular disease

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4
Q

Type 1 major cause of death

A

Chronic kidney disease

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5
Q

Type 2 major cause of death

A

MI, CVA

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6
Q

What is 2-4x higher in diabetes?

A

Heart disease and stroke

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7
Q

GDM and future diabetes

A

Increases mom’s risk by 40% over 20 years

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8
Q

Which type is more prone to ketoacidosis?

A

Type 1

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9
Q

Type 1A

A

Lymphocytic attack on beta cells

Central to pathology

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10
Q

Type 1B

A

Idiopathic

Inflammation but no antibodies

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11
Q

LADA

Latent autoimmune diabetes of adulthood

A

Autoantibodies
Adult age
Don’t need insulting in first 6 months after dx

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12
Q

Classic new onset of T1DM

A

Hyperglycemia without acidosis

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13
Q

Most important contributor of insulin resistance

A

Obesity!! Visceral fat more

Bad adipokines- TNF and resistin

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14
Q

Metabolic syndrome

A 
3 more more of the following:
Insulin resistance
Increase TG
low HDL
HTN
Apple shape
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15
Q

Early T2DM

A

Hyperplasia of beta cells

Fasting hyperinsulinism

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16
Q

Progression of T2DM

A

Hypoinsulinemia eventually, beta cell function eventually poops out

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17
Q

If you only rely on fasting glucose…

A

You will miss a ton of patients with diabetes

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18
Q

MODY

Maturity onset diabetes of the young

A

Rare, mild form of non insulin dependent diabetes

Autosomal dominant inheritance, less than 25 years old

Impaired glucose induced secretion of insulin

Not obese, few microvascular complications

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19
Q

Kussmaul

A

Respirations of DKA

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20
Q

OGTT

A

Best to detect T2DM at an earlier stage

Carb restriction, then 8 hour fast

Blood draw at zero and 120 minutes

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21
Q

HbA1c

A

Diagnostic

Reflects blood sugar levels over preceding 8-12 weeks and mostly previous month

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22
Q

Serum fructosamine

A

Evaluates glucose levels in the preceding 1-2 weeks, esp…

During pregnancy
Monitoring recent changes in treatment
Hemoglobinopathies

**greatly affected by serum albumin levels

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23
Q

Criteria for DM diagnosis

A

fasting plasma glucose: >126

2 hour OGTT: >200

HbA1c: >6.5

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24
Q

Dianogisis made after…

A

Repeat test on another day or two different diagnostic tests on the same day

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25
Q

Ketonuria suggests…

A

Type 1

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26
Q

Diabetic retinopathy

A

Most common in type 1, will 100% have it after 30 years

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27
Q

Nonproliferation diabetic retinopathy

A

Most common cause of visual impairment of T2

Earliest stages, usually nosymptoms

Dot hemorrhages, exudates

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28
Q

Proliferative diabetic retinopathy

A

Leading cause of blindness in US

New, fragile capillaries that cause hemorrhages

Retinal detachment

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29
Q

Retinopathy management

A

T1’s after 3-5 years

T2’s at time of diagnosis and annually

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30
Q

Diabetic nephropathy

A

More common in type 1

Microalbuminuria/proteinuria

2 out of three tests abnormal over 3-6 months to make diagnosis

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31
Q

Diabetic nephropathy tests

A

Micoalbuminuria: 30-300

Proteinuria >300

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32
Q

Distal symmetric neuropathy

A

Most common

Stocking glove pattern, longer nerves more vulnerable

Delayed sensory and motor nerve conduction

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33
Q

Distal symmetric neuropathy findings

A

Bilateral and symmetric dulled perception of vibration, pain and temperature

Callus and ulceration formation, high pressure areas

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34
Q

Charcot arthropathy

A

Develops from untreated neuropathy and trauma

Rocker bottom deformity, joint subluxation and periarticular fractures

Osteoclastic destruction and deraned/unstable joints in the mid foot

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35
Q

Isolated peripheral neuropathy

A

Sudden onset with subsequent recovery

Vascular ischemia or traumatic damage

Cranial or femoral nerves

**motor abnormalities predominate

Self. Limited!

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36
Q

Painful diabetic neuropathy

A

Mild or severe, tends to be at night

Sensory disturbances, progressive positive symptoms like…
Burning, hot poker
Deep, aching pain
Creepy crawlies

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37
Q

Autonomic neuropathy

A

Dysfunction of ANS due to poor glucose control and vascular risk factors

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38
Q

CV neuropathies

A

Exercise intolerance, OH, tachy, silent MI

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39
Q

Peripheral autonomic dysfunction

A

Changes in skin, itching
Edema, venous prominence
Callus, loss of nails, sweating

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40
Q

GI autonomic neuropathy

A

Esophageal motility

Gastroparesis

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41
Q

GU autonomic neuropathy

A

Bladder dysfunction
Retrograde ejaculation
ED
Dyspareunia

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42
Q

CV complications of DM

A

MI is the leading cause of death in T2

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43
Q

PVD in DM

A

Atherosclerosis is markedly accelerated

Ischemia of lower extremities

Gangrene!

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44
Q

Traetment of gangrene

A

Avoid tobacco!!

Avoid propranolol

Debridement

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45
Q

Sporadic monitoring

A

<1 time per day

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46
Q

Systematic monitoring

A

1-2 times per day

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47
Q

Block monitoring

A

Up to 8 times a day for 3-4 days in a row, 1-2 blocks per month

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48
Q

Postprandial monitoring

A

2 hours after a meal

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49
Q

Intensive daily monitoring

A

Greater than 4 times per day

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50
Q

Limitations of glucometers

A

Need to be calibrated
Less accurate numbers if at extremes
Real time readings not always accurate

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51
Q

Con of continuous glucose monitor

A

30 minute sensor lag

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52
Q

Diabetics hospitalized

A

Stress induced changes

Insulin preferred in this setting, easier to match with individual needs

Morbidity and mortality is twice that of non diabetics

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53
Q

DKA triad

A

Hyperglycemia
Ketonemia
Anion gap metabolic acidosis

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54
Q

develop DKA from 3 factors

A

Insulin deficiency
Increased counterregulatory hormones
Dehydration

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55
Q

DKA presentation

A

Coma
Marked fatigue/weakness
NV
Weight loss

Kussmaul breathing
Fruity breath
Tachy, HOTN

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56
Q

DKA goals of treatment

A

Restore plasma volume and tissue perfusion

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57
Q

Levels of DKA treatment

A

Mild- treated in ED

Moderate- admit to hospital, alert or drowsy

Severe- admit to hospital, stupor/coma

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58
Q

Fluid replacement in DKA

A

Cornerstone of treatment- shortcome of traetment is usually failure to restore normal perfusion

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59
Q

If BS around 250…

A

Change IVF to 5% glucose in order to prevent hypoglycemia and cerebral edema

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60
Q

Sodium bicarbonate replacement

A

Repeat until pH is 7.1 then discontinue

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61
Q

Hypoglycemia in diabetics occurs…

A

When BS drops below 60 from

Over medication
Fasting
Exercise
Insulin adjustment

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62
Q

Hypoglycemia presentation

A

Tachy, palpitations, sweating, tumor

Nausea, hunger

Confusion, difficulty speaking, blurred vision, headache, seizures, LOC

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63
Q

Hypoglycemic unawareness

A

Repeated episodes of hypoglycemia causing an adaptive process

Neuroglycopenic symptoms first, need to keep BS high for several weeks

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64
Q

Insulinomas causing hypoglycemia

A

Adenoma of islets of langerhands, usually single and benign

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65
Q

Whipple triad

A

Pancreatic beta cell tumor presentation

Hx of hypoglycemic symptoms
Fasting BS less than 45
Glucose administration leads to immediate recovery

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66
Q

Critical diagnostic test of beta cell tumor

A

Inappropriately elevated serum insulin levels at time when hypoglycemia is present

Elevated proinsulin and c peptide

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67
Q

Postprandial alimentary hypoglycemia

A

Rapid gastric emptying of food after gastrectomy procedures causing reactive hypoglycemia

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68
Q

NIPHS aka islet cell hyperplasia

A

Hyperinsulinemic hypoglycemia AFTER MEALS but not with fasting (unlike beta cell tumors)

Positive calcium stimulated angiography

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69
Q

Functional alimentary hypoglycemia

A

Increased sympathetic activity after meals

Everything WNL

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70
Q

Occult diabetes

A

Exaggerated insulin release occurs after initial hyperglycemia from GTT

Potential diabetics

Weight loss and reduced carb diet

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71
Q

Immunopathologic hypoglycemia

A

Anti insulin antibodies (more common)
Antibodies to insulin receptors (extremely rare)

3-4 hours after meals

High insulin levels and titers of insulin antibodies

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72
Q

Production of thyroid hormone controlled by…

A

Iodine intake

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73
Q

T3 versus t4

A

T3 is more active than t4

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74
Q

TSH

A

Best initial lab for screening

Used to monitor traetment of hypothyroid

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75
Q

Free t4

A

Gives an earlier picture of function

Monitors efficacy of treatment in hyperthyroid

76
Q

Most common cause worldwide of hypothyroid

A

Iodine deficiency

77
Q

Most common cause where adequate iodine intake of hypothyroid

A

Hashimoto

78
Q

Drug induced hypothyroid

A

Amiodarone

Lithium

79
Q

Hypothyroid presentation

A 
Fatigue
Cold intolerant
Constipation
Dry skin
Cramping
Menorrhagia 
Depression
80
Q

Primary hypothyroid diagnosis

A

High TSH

Low free t4

81
Q

Secondary hypothyroid

A

Low or normal TSH

Low or normal free t4

82
Q

Sub clinical hypothyroid

A

Elevated TSH

Normal free t4

83
Q

Myxedema crisis

A

Severe hypothyroid

AMS, hypothermia, bradycardia, hyponatremia

Emergent!

84
Q

CHF and CAD can be exacerbated by…

A

Levothyroxine

85
Q

Hyperthyroid presentation

A 
Nervous, anxious
Heat intolerance
Palpitations
Sweating
Weight loss
Loose stool
Amenorrhea
Tremors
86
Q

Graves’ disease

A

Goiter and thyrotoxicosis
Autoimmune
20-40
Proptosis

87
Q

Toxic multinodular goiter

A

Iodine deficient areas
Enlarged thyroid with multiple nodules

> 65 years old

88
Q

Toxic nodule- adenoma

A

Younger patients, autonomously functioning thyroid nodule

89
Q

Subacute thyroiditis

A

Benign

Viral infections usually

Painful, swollen thyroid

Elevated ESR

Thyrotoxicosis for about 3-6 weeks

90
Q

Postpartum thyroiditis

A

Autoimmune, thyrotoxicosis 2-6 weeks postpartum for up to 12 weeks

Anti TPO positivity is predictive

Painless goiter, can develop permanent hypothyroid

91
Q

Silent thyroiditis

A

Anti thyroid antibodies possibly

Medication or spontaneous trigger

92
Q

Amiodarone induced hyperthyroid

A

Contains a lot of iodine, can happen up to 3 years after stating medication

Produces a destructive autoimmune process

93
Q

Hyperthyroid labs

A

Low TSH
High t4 (or normal)
High t3

94
Q

Graves labs

A

TSI elevated

Anti thyroid peroxidase significantly elevated

95
Q

Thyroid storm

A

Rare

Fever, tachy, CNS dysfunction, dehydration, delirium

No time for labs, treat! Hypermetabolic state

96
Q

Complications of hyperthyroid

A

Arrhythmias
Hypercalcemia
Osteoporosis

97
Q

Triphasic course of thyroiditis

A

Thyrotoxic, hypothyroid, recovery

98
Q

Hashimotos features

A

High anti TPO

Has a relation to celiac

30-50 years old

99
Q

Suppurative thyroiditis

A

Immunosuppression

Fever, pain, fluctuation, tender thyroid

Elevated ESR, abscess

100
Q

Riedel’s thyroiditis

A

Systemic fibrosis, 30-60 years old

Rock hard goiter, esophageal or tracheal impression

Hypothyroid from scar tissue in gland

101
Q

Endemic goiter

A

Low dietary iodine intake

Impaired thyroid hormone synthesis and hyperplasia of thyroid tissue, can be euthyroid

Compressive symptoms

102
Q

Anterior pituitary function

A

Synthesizes and realizes peptide hormones

103
Q

Posterior pituitary function

A

Secretes nuerohormones made in hypothalamus

104
Q

Infindubulum

A

Attaches hypothalamus and pituitary

105
Q

Sella turcica

A

In sphenoid bone, where the pituitary plans sits (just below optic chiasm)

106
Q

Anterior gland receives…

A

Hormone signals

107
Q

Posterior glad receives…

A

Direct tracts from hypothalamus

108
Q

Posterior gland hormones

A

Oxytocin

ADH aka vasopressin

109
Q

Somatostatin is…

A

Inhibitory

110
Q

Acromegaly/gigantism general

A

Excess growth hormone

Usually pituitary adenoma

Acromegaly is after the epiphyseal plates close

111
Q

Acromegaly presentation

A 
Large doughy hands
Widened fingers, feet, head
Coarse facial features
Spreading teeth
Amenorrhea
112
Q

Temporal hemianopia

A

Peripheral vision loss due to compression of optic chiasm by mass

Any pituitary mass can do it, seen in acromegaly

113
Q

Labs in acromegaly/gigantism

A

IGF-1 is always elevated. If its not, this is ruled out

Glucose challenge with measured GH if high IGF

114
Q

Imaging with pituitary

A

Always MRI of sella turcica

> 10 mm is macro

115
Q

Acromegaly traetment

A

Transsphenoid approach for surgery

Medical management with DA agonists or somatostatin analogs

116
Q

Incidentaloma pituitary

A

Check prolactin
GH
ACTH

All to rule out hypersecretion

Then image or monitor

117
Q

Dwarfism general

A

GH deficiency of anterior pituitary secretion in childhood

Generally don’t undergo puberty

118
Q

Achondroplastic dwarfism

A

Different from GH deficiency, this is cartilage not being converted to bone

119
Q

Prolactinoma

A

Hyperprolactinemia from pituitary tumor

In females could have infertility, galactorrhea, amenorrhea

Males, infertility, gynecomastia, etc.

120
Q

Anterior hypopituitarism

A

Partial or complete deficiency of one or more pituitary hormones

Hypothalamus or pituitary dysfunction

*hormone substitution

121
Q

Pituitary apoplexy

A

Sudden neurological impairment, like HA, visual changes, AMS, hormonal abnormalities

Hemorrhagic or ischemic

High dose steroids!

122
Q

Cortex zones

A

Glomerulosa
Fasciculata
Reticularis

123
Q

Glomersulosa

A

Aldosterone

124
Q

Fasciculata

A

Cortisol

125
Q

Reticularis

A

Estrogen/androgen

126
Q

Medulla

A

Secretes catecholamines, like epinephrine and NE

127
Q

Aldosterone

A

Salt retention to regulate blood pressure, suppression of renin

If excess, HTN, hypokalemia, cardiac events

128
Q

Test all HTN patients with hypokalemia for…

A

Aldosterone levels and plasma renin activity

129
Q

Conn syndrome

A

Hyperaldosteronism from adrenal adenoma secreting aldosterone

130
Q

Random potential cause of hypokalemia

A

Black licorice

131
Q

Most common cause of refractory HTN in young/middle aged patients?

A

Hyperaldosteronism

132
Q

Adrenal insufficiency

A

Basically cortisol insufficiency with or without mineralocorticoid deficiency

133
Q

Primary adrenal insufficiency

A

Addison’s disease

Adrenal absence or dysfunction

134
Q

Secondary adrenal insufficiency

A

Deficienct secretion of ACTH

135
Q

Acute adrenal crisis

A

Emergency!

Could be stress, acute ACTH deficiency, etc

136
Q

Adrenal insuffiency presentation

A

Weakness, abd pain, fever, confusion, hypotension, hyperkalemia, hyperpigmenttion

137
Q

ACTH stimulation test

A

For adrenal insufficiency

Pre test serum cortisol, then administer synthetic ACTH

Cortisol Should double within an hour

138
Q

Cushing syndrome

A

Hypercortisolemia

Obesity, striae, osteoporosis, HTN, leukocytosis, hypokalemia, moon face, buffalo hump, glaucoma

139
Q

Testing for cushing’s

A

Dexamethasone suppression test

Give dexamethasone at 11 pm, check cortisol at 8 am

If a low cortisol, then diagnosis excluded

140
Q

Follow dexamethason suppression test with…

A

24 hour free urine cortisol and creatinine

141
Q

Pheochromocytoma

A

Tumor arising from adrenal medulla

Produces catecholamines

142
Q

Pheochromocytoma presentation

A

Classic triad of severe HA, tachy/palpitations, perspiration

Bursts of NE and epi, the symptoms that go along with that

143
Q

Adrenal cancer

A

A non functional tumor >6 cm is highest risk

Varied endocrine presentations

144
Q

Adrenal hemorrhage

A

Pain is the major symptom

CT imaging

145
Q

Multiple endocrine neoplasia (MEN)

A

Autosomal dominant inheritance

Multiglandular endocrine tumors, can develop at any time

146
Q

Calcium homeostasis general

A

Ca modulates neuron permeability to sodium

Hypocalcemia causes hyperexcitability

Hypercalcemia depresses neuronal activity

147
Q

Parathyroid hormone

A

Released in response to low calcium levels

Causes bone resorption(osteoclast activity)
Renal reabsorption
Increased intestinal absorption

148
Q

Calcitrol

A

Produced in kidney in response to PTH

Active form increases GI absorption of calcium

149
Q

Calcitonin

A

Produced in thyroid

Opposite effect of PTH

Decreases bone resorption, increases renal excretion

150
Q

Hypoparathyroidism

A

Hypocalcemia

Can be caused by many things

151
Q

Acute hypoparathyroidism presentation

A 
Tetany
Muscle spasms, cramps
Stridor
Tingling 
AMS
Convulsions
152
Q

Chronic hypoparathyroid presentation

A

Lethargy or anxiety
Cataracts
EKG changes- prolonged QT
Or asymptomatic!

153
Q

Chvostek sign

A

Facial twitch with tapping facial nerve

Related to hypocalcemia

154
Q

Trousseau phenomenon

A

Carpal spasm with BP cuff inflation sustained for 2-3 minutes

Associated with hypocalcemia

155
Q

Labs in hypoparathyroidism

A

Decreased serum calcium
Increased serum phosphate
Decreased urinary calcium

Low PTH

Serum ca is highly protein bound, so check free Ca

156
Q

Pseudohypoparathyroidism

A

Congenital renal resistance to PTH

Hypercalcuria
Hypocalcemia
Increased bone resorption

PTH still behaving normally at the level of the bone

157
Q

Pseudohypoparathyroidism presentation

A 
Osteodystrophy
Short stature
Ectopic bone formation
Short 4th metacarpal
Hypocalcemia
158
Q

Hyperparathyroidism

A

Most common cause of hypercalcemia

Hypersecretion of PTH, usually single adenoma but could be more

159
Q

Secondary hyperparathyroidism

A

CKD or dialysis, not great renal function so phosphate not getting excreted

Makes the parathyroid glands think the body is hypocalecemic

160
Q

Tertiary hyperparathyroidism

A

Stimulated glands from secondary become large and autonomous

161
Q

Parathyroid carcinoma

A

Extreme hypercalcemia

Half are palpable

Half are extended locally or have mets

162
Q

Hyperparathyroidism presentation

A

Bones, stones, abdominal groans, psychics moans with fatigue overtones

Increased bone resorption, brown tumors, compression fractures
Kidney stones
Constipation, NV
Depression, AMS
Fatigue, malaise, weakness
163
Q

Labs of hyperparathyroidism

A

Elevated serum calcium

Normal or elevated urine calcium

164
Q

Calciphylaxis

A

Tertiary hyper PTH due to CKD

Calcification of skin, soft tissue, and arteries

Necrosis and gangrene, arrhythmia and respiratory failure

165
Q

Post op secondary hyper PTH

A

Transient, due to hungry bones that soak of Ca

Persistently low Ca triggers PTH release

166
Q

Osteoporosis

A

Reduced bone mass/integrity leading to fx risk

Most common in postmenopausal women

167
Q

Osteoporosis manifestations

A

Backache

Loss of height- vertebral fractures, dowagers hump

168
Q

Osteoporosis diagnostics

A

DEXA scan, usually lumbar spine and hip, reports a T score

169
Q

T scores

A

Normal- >-1
Low bone mass- -1 to -2.5
Osteoporosis- less than or equal to -2.5

170
Q

Screening for osteoporosis

A

DXA screening of women greater than 65, or below 65 with increased risk

The worse the T score, the more often you have to get a DXA

171
Q

Osteomalacia

A

Defective mineralization of bones

Rickets in peds

172
Q

Osteomalacia cause

A

Vitamin D deficiency is the most common

Anything that disrupts Ca and or phos mineralization of the bone

173
Q

Paget disease of bone

Osteitis deformans

A

Excess bony mass but with poor integrity

Bone pain, tibial bowing, chalfstick fractures

174
Q

Osteogenesis imperfecta

A

Type 1 collagen mutation

Severe osteoporosis

Spontaneous fx in utero or childhood

Blue ish sclera

175
Q

Odds higher for thyroid cancer in…

A

Nodules found in young patients

176
Q

Symptoms of thyroid nodules

A

Rare

Goiter
Cervical LAD
Hoarseness (recurrent laryngeal n compression)
Dyspnea
Superior vena cava syndrome
177
Q

Thyroid nodule imaging

A

Ultrasound! First line

178
Q

Thyroid scintigraphy does not…

A

Distinguish benign versus malignant

Cold nodules 5-10% are malignant, FNA recommended

Hot nodules are less likely to be cancer

179
Q

Thyroid nodule therapy

A

Levothyroxine, therapeutic if increased TSH

Can use with normal TSH because reduces development of new nodules. Needs to be >2 cm

Surgery if malignant

180
Q

Mets in thyroid cancer

A

Nodes
Lung
Bone

181
Q

Papillary thyroid cancer

A

Most common
30-50 years

Solitary or multifocal

Can easily spread

182
Q

Papillary thyroid cancer prognosis

A

Good, even if advanced

Just need to treat

183
Q

Follicular thyroid cancer

A

Less common, more aggressive
40-60

Can cause hyperthyroidism
Elevated serum thyroglobulin

Better differentiation, less risk of mets and better prognosis

184
Q

Medullary thyroid cancer

A

Parafollicular cells
Secrete calcitonin, CEA and others (markers for cancer)

Thyroid function is normal

Can present with flushing and diarrhea

185
Q

Anaplastic thyroid cancer

A

Undifferentiated and explosively aggressive

Always stage IV diagnosis

186
Q

4 t’s of anterior mediastinal mass

A

Thymus
Teratoma
Terrible lymphoma
Thyroid

Clin Med 2 (8 decks)

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