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PCM Midterm 2020 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is the pathophysiology for diabetes mellitus type 2?

A

Insulin resistance leading to ineffective transport of glucose leading to hyperglycemia leading to end organ damage

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2
Q

What are the common complications of DM2?

A

Remember: MIM

  • Microvascular: retinopathy (blurred vision) neuropathy (tingling in extremities)
  • Macrovascular (stroke, MI, Peripheral vascular disease)
  • Increase in Infections (unusual infections) (necrotizing fasciitis)
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3
Q

Management of DM2?

A

Lifestyle changes
Oral metformin
Insulin

Check HbA1c every 3 months, 6 months once more stable

OTHER: Smoking cessation, BP control, hyperlipidemia control

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4
Q

What are the risk factors for DM2?

A 
Over 45 years old
BMI over 25
DM type 2 in First degree relative
high risk ehtnicity (AA, hispanic..)
gestational diabetes history
hypertension
dyslipidemia
LABS: HbA1c > 5.7
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5
Q

Clinical presentation of DM2

A 
Polyuria
Polydypsia
Polyphagia
Acanthosis nigricans
Foot ulcer
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6
Q

What is acanthosis nigricans

A

black/ grey neck ring line in DM2

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7
Q

what is the ADA criteria for DM2 diagnosis?

A

HbA1C >6.5
Fasting Glucose>126
2 hour glucose > 200
Random glucose >200 with classic hyperglycemia symptoms

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8
Q

What do you look for in a diabetic foot exam?

A

Callus/corn formation, breaks in skin, erythema, dryness
Check pulses
Check sensation

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9
Q

What is DKA? How does it present?

A

Associated with type one but can present in type 2
Clinical presentation: nausea, vomitting, abdominal pain, dehydration, fruity smelly breath kussmaul respirations (deep respirations, using accessory muscles)

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10
Q

What are the typical lab characteristics of DKA? and HHS? (HHS= Hyperosmolar Hyperglycemic State, aka marked hyperglycemia)

A

DKA/Hyperglycemia: blood glucose > 200

HHS: Glucose > 600

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11
Q

What is the management for DKA and HHS?

A

Admittance to hospital for IV fluids, IV insulin, K replacement
DO NOT MANAGE AS OUTPATIENT

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12
Q

What is the pathophysiology for diabetes mellitus type 1?

A

Polydipsia, polyuria, weight loss with hyperglycemia and ketonemia or ketonuria, DKA
HAPPENS IN CHILDHOOD (normal presentation)

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13
Q

What are some major differences between DM1 and DM2? Onset? Age? Ketosis? Insulin dependence? Pancreatic antibodies?

A

1: Childhood, acute severe onset, ketosis is common, strong associate with HLA-DR3/4, Decreased or absent insulin decrease –> dependent on insulin, pancreatic antibodies found
2: present around puberty, onset insidious to severe, 5-10% present with DKA, no associate with HLA-DR3/4, No pancreatic antibodies, normally patients overweight and have acanthosis nigricans

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14
Q

Associated conditions of DM1

A

Autoimmuen thyroiditis
celiac disease
addisons disease

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15
Q

Management of DM1

A

Education
Insulin
IV insulin or IV hydration may be necessary

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16
Q

What is metabolic syndrome? (diagnosis as defined by the ATPIII)

A 
ATP3 (any 3 of the following):
abdominal obesity
triglycerides over 150
HDL over 40 for women, 50 for men
BP over 130/85
Fasting glucose >100

THINK: BHFAT

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17
Q

what conditions are associated with Metabolic syndrome?

A

polycystic ovary syndrome
obstructive sleep apnea
nonalcoholic fatty liver disease, hyperuricemia

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18
Q

how do you manage Metabolic syndrome?

A

Lifestyle changes!!!! (diet, exercise)
weight loss medication or surgery
statin medication, BP medication, metformin

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19
Q

What parts of the history are very important for DM1, DM2, and metabolic syndrome?

A 
Weight gain/loss
urinary frequency
excessive thirst
numbness and tingling
vision changes
fatique
slow healing
diet (feeling hungry constantly)
exercise (limited or nonexistent)
history of gestational diabetes
family history
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20
Q

What are the risk factors for Metabolic syndrome?

A 
Overweight/obesity
sedentary lifestyle
genetics
aging
DM Type 2
CVD
Lipodystrophy
21
Q

What are common causes of endocrine dysfunction?

A

1) Hormone excess (neoplastic growth, autoimmune, excessive administration)
2) hormone deficiency (autoimmune destruction, tumor, surgery, infection, hemorrhage, infection, inflammation)
3) hormone resistance (inherited)

22
Q

What are the dynamic tests of endocrine testing? What are (Generally) the two treatments for endocrine dysfunctions?

A

1) Suppression tests: assess endocrine hyperfunction
2) Stimulation: assess endocrine hypofunction

1) Replace deficient
2) Suppress excessive

23
Q

What screening or testing recommendations are recommended for:

1) Hypothyroidism
2) Graves
3) Thyroid nodules
4) Hyperparathyroidism

A

1) Hypothyroidism: TSH, confirm with free T4 (screen woman after 35 and every 4 years)
2) Graves TSH, free t4
3) Thyroid nodules (physical exam, fine needle aspiration biopsy)
4) Hyperparathyroidism (serum calcium, PTH if calcium elevated)

24
Q

What is the clinical presentation of hyperthyroidism?

A

Weight loss, anxiety, diaphoresis, heat intolerance, palpitations, amenorrhea, tremor, increased appetite, frequent bowel movements, proximal muscle weakness

25
Q

Potential causes of hyperthyroidism?

A

Graves disease
subacute (De quervain’s) thyroiditis (often see postpartum, will transition into hypo phase)
Amiodarone (a drug, can also cause hypothyroidism)

26
Q

What should you exam if your concerned about the thyroid?

A

THE LUNGS

27
Q

What is the clinical presentation of hypothyroidism?

A

fatigue, weight gain, anorexia, dry coarse skin, cold intolerance, weakness, muscle cramps, impaired memory,d epressed mood, hearing change, diminished sweating, voice hoarseness

28
Q

Potential causes of hypothyroidism?

A

Hashimoto’s thyroiditis
Iodine deficiency (Rare in developed world now)
subacute (De quervain’s) thyroiditis (often see postpartum, start hyper)
Lithium (drugs for bipolar disorder)

29
Q

What is the classic graves presentation?

A

proptosis or

exopthalmos

30
Q

What is the classic presentation of classic primary hyperparathyroidism?

A

BONES (bone pain, osteopenia/osteoporosis), STONES (polyuria, polydipsia, nephrogenic diabetes inspidus), ABDOMINAL MOANS (anorexia, nausea vomitting, peptic ulver, pancreatitis, constipation), AND PSYCHIC GROANS (decreased concentration, confusion, fatigue)

Bone disease, hypercalcemia, hypophosphatemia, hypomagnesemia, anemia, gout

31
Q

Describe PTH signaling

A

Decreased serum calcium stimulates release of PTH from parathyroid glands, those act on kidney and bone directly and intestine indirectly (through Vit D)

32
Q

How do you assess for hypocalcemia? classic presentation?

A

Trousseau’s sign: carpopedal spasm (this one is better, both kinda worthless)
Chvostek’s contraction of facial muscles elicited by tapping facial nerve just anterior to the ear (high chance of false negative)
other findings: cataracts, dry coarse skin, hyperpigmentation, eczema, steatorrhea

33
Q

What symptoms of primary hyperparathyroidism are mostly due to the PTH excess? Which ones are due to the hypercalcemia?

A

PTH excess: nephrolithiasis, bone disease

hypercalcemia: anorexia, nausea, constipation, polydipsia, polyuria

34
Q

Potential causes of hyperparathyroidism

A

Parathyroid: adenoma, hyperplasia, carcinoma (rare)
Multiple endocrine neoplasia (MEN syndromes)
Chronic renal failure: secondary, or tertiary, form of HPTH

35
Q

Clinical presentation of hypoparathyroid, hypocalcemia?

A

Neuropsych: seizures, dementia, anxiety, depression
Neuromuscular: paresthesia round mouth and fingers, myalgia, spasms
CV: hypotension
Autonomic: biliary colic, diaphoresis
Other: cataracts, hyperpigementation

36
Q

Causes of hypoparathyroid, hypocalcemia?

A

surgical removal of glands during thyroidectomy
DiGeorge Syndrome
Hereditary auoimmune syndrome

37
Q

What happens where there is an excess of cortisol? what about ACTH from pituitary?

A

Cortisol excess: cushing’s syndrome

hypersecretion ACTH: Cushing’s disease

38
Q

What does cushings syndrome present with?

A

overproduction of cortisol or ingestion of exogenous corticosteroids:
HTN, central ovesity, hirsutism, striae, eccymosis

39
Q

What causes adrenal insufficiency? (Primary and secondary?)

A

Primary: Addison’s
Autoimmune, surgical removal, If you have HIV AND TB this is it!!!
Second: pituitary failure, exogenous steroids

40
Q

What is the clinical presentation of adrenal insufficiency? (Addisons)

A

• Hyperpigmentation • Weakness • Fatigue • Anorexia • Nausea and vomiting • Hypotension • Salt craving • Syncope

41
Q

What is (Are) the clinical pearl(s) of Addison’s disease

A

Skin and oral mucosa hyperpigmentation, hypotension

42
Q

What are some major causes of hypopituitarism?

A

HYPOTHALAMIC DISEASES
Mass lesions (metastatic from lung, breast), radiation, infiltrative lesions, infections, traumatic brain injury)
PITUITARY DISEASES
Mass legions (pituitary adenomas), pituitary surgery, radiation, infection, infaraction, genetic mutations

43
Q

How does the thyroid feel to palpation in graves? hashimotos thyroiditis and lignancy? thyroiditis?

A

graves? soft
hashimotos? firm
thyroiditis? tender

44
Q

What does a PT do for you to inspect their thyroid?

A

isthmus overlies 2-4 tracheal rings, flex neck slightly to relax SCM, place fingers just below cricoid cartilage, displace trachea to one side and palpate that lobe

45
Q

When might you hear a bruit in the thyroid?

A

hyperthyroidism or toxic multinodular goiter

46
Q

How do you complete a diabetic foot exam

A
  1. Examine the feet for skin lesions/infection, etc. (don’t forget to check between the toes)
  2. Pressure sensation using Monofilament testing
  3. Vibration sensation testing using a tuning fork
  4. Superficial pain sensation using
    pinprick/temperature sensation
  5. Bilateral DTRs of the ankle
  6. Bilateral pulses (dorsalis pedis, posterior tibial)
47
Q

where should you do the 10-g monofilament sensation testing

A

big toe
three spots on pad of foot
heel of foot
(pinkie toe too)

48
Q

How do you interpret glucose testing? What results do you see in a normal fasting glucose? 2hr post prandial glucose? random glucose?

A

Normal Fasting Glucose: <100 mg/dL Normal 2 hr Post-Prandial Glucose: <140 mg/dL Normal Random Glucose: <200 mg/dL

PCM Midterm 2020 (6 decks)

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