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Endocrine Flashcards

1
Q

Thyroid Development

A
  • Deriative of floor of ectoderm, descends along thyroglossal duct to sit in anteior midline.Foramen Cecum
  • Thyroid along duct leads to pyramidal lobe
  • Ectopic thyroid is located at base of tongue
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2
Q

Thyrglossal duct cyst

A
  • Located anterior midline and moves with swallowing

- Branchial cleft cysts are located laterally

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3
Q

Fetal Adrenal Gland

A
  • Contains fetal part that secretes sex steroids
  • Adult part which secretes Cortisol under influence of fetal ACTH.
  • Cortisol is crucial for lung development and surfactant production
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4
Q

Zona Glomerulosa

A

-Most cortical, secretes aldosterone in response to renin-angiotensin 2

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5
Q

Zona Fasicularis

A

-Secretes coritsol in response to ACTH/CRH

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6
Q

Zona Reticularis

A

-Secretes Sex steroids, also increased by ACTH and CRH

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7
Q

Adrenal Medulla

A

-Contains NC derived chromafin cells (S-100 +) that secrete Epi (some nor epi, 10%) in response to Ach releaased from preganglionic sympathetics that branch from IML at T10-L1 and travel along splanchinics

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8
Q

Pheochormocytoma

A
  • Tumor of adrenal medulla in adults causes episodic HTN

- Located with MBIG scan which will detect location of ectopic caetacholamine synthesis

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9
Q

Neuroblastoma

A

Kids

  • Most common location is adrenal medulla, does not cause episodic HTN Most common extracranial mass in childhood
  • MBIG scan will localize ectopic caetacholamine secretion.
  • Can spread and involve any location along sympathetics or elsewhere
  • Increased risk with NF-1 and Beckwith wiederman
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10
Q

Arterial Supply of Adrenal

A
  • Superior adrenal off phrenic
  • Middle adrenal off aorta
  • Inferior adrenal off Renal
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11
Q

Venous Drainage

A
  • L: Adrenal drains dircetly into IVC

- R: Adrenal drains to renal the to IVC

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12
Q

Posterior Pituitary

A
  • Derivative of neuroectoderm
  • Recieves inputs from magnocellular neurons that originate in supraoptic and paraventricular hypothalamus. (near disrutpion in BBB called OVLT that senses osmolality)
  • Secretes ADH and Oxytocin, carried along magnocellular neurons by neurophysin
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13
Q

Anterior Pituitary

A
  • Derivative of surface ectoderm (Rathkes pouch)
  • Acidophilic cells: GH and Prolactin
  • Basophilic: FSH, LH, ACTH, TSH
  • TSH, FSH, LH, HCG have similiar alpha subunit, beta subunit determines specificity
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14
Q

Endocrine Pancreas

A

Islets of langerhans

  • Alpha (glucagon) Peripherally located
  • Beta (insulin) Centrally located
  • Delta (somatostatin) Interspersed
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15
Q

Insulin Physiologic Release

A

-Elevated glucose enters beta cells through Glut-2 which is high capacity but low affinity. Increase glucose leads to increase ATP. Elevated ATP closes K channel leading to depolarization, opening of V-gated Ca channels which signal release of insulin.

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16
Q

Insulin Secreted hormonally

A
  • Beta 2 increases insulin secretion
  • Glucagon stimulates Gs which also increases insulin secretion
  • GH also increases insulin secretion
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17
Q

Insulin sepressed hormonally

A
  • Supressed by alpha 2 stimulation

- Also suppressed by somatostatin

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18
Q

Glut -1

A

Insulin independent

  • Enriched in brain and RBC
  • Low capacity and high affinity (basal levels take up)
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19
Q

Glut - 2

A
  • Insulin independent
  • Increased in Liver, Beta Cells, Kidney, Small intestine.
  • Low affinity but high capacity. With high glucose levels large quantities will enter cells
  • Responsible for insulin secetion and for bringing glucose levels down after meal
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20
Q

Glut - 4

A

Insulin Dependent

  • Enriched on skeletal muscle and adipose (Storage depots)
  • also present on cardiac tissue
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21
Q

Insulin effects on electrolytes

A
  • Causes increase in Na/K ATPase which brings K in and decreases extracellular K
  • Causes Na retention by kidney
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22
Q

Proinsulin

A

Secreted as disulfide bridged dimer with C peptide

-Can be used to see if insulinoma or facticous

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23
Q

Glucagon

A

-Released from alpha cells in response to hypoglycemia

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24
Q

Theraputic uses of glucagon

A

-Can be used to treat beta blocker overdose. Both are Gs receptors

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25
Q

TRH effects

A

-Causes release of prolactin and TSH

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26
Q

Prolactin

A

-Inhibits GnRH

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27
Q

CRH

A

Causes release of POMC

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28
Q

Prolactinoma effects

A
  • No periods while breast feeding

- Amenorrhea with PRL secreting tumor

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29
Q

Prolactin Functions and regulation

A
  • Causes increaed milk production in female
  • Inhibits GnRH leads to no periods during breast feeding, amenorrhea, no spermatogenesis
  • Inhibited by dopamine (severe stock leads to increase)
  • Stimulated by estrogen (OC) and TRH (hypothyroid)
  • Prolactincomas treated with dopamine agonists (pergolide, bromocriptine)
  • Antipsychotics (dopamine antagonists) and OC can cause galactorrhea
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30
Q

GH

A
  • Produced by aciophils in AP
  • Stimulated by GHRH
  • Inhibited by high glucose and somatostatin
  • Causes the release of IGF-1 from liver which stimulates linear growth
  • Tumor leads to gigantism in kids and acromegally in adults. (most commonly die of Heart Failure)
  • Test with glucose supression and can also measure IGF-1 levels
  • Tumor treated with somatostatin analog octreotide
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31
Q

Adrenal steroid production

A
  • Begins at cholesterol. Desmolase is rate limiting step which produces pregnenalone. Desmolase increased by ACTH and inhibited by ketocolanazole
  • 17 hydroxylase makes sex steroids an cortisol
  • 21 hydroxylase makes cortisol and aldosterone
  • 11 hydroylase makes cortisol and aldosterone
  • Angiotensin 2 stimulates aldosterone synthase
  • CAH is absence of one of these enzymes which leads to hypersecrtion on ACTH from low cortisol levels leading to enlarged adrenals
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32
Q

17 Deficency

A
  • Leads to impaired sex and cortisol production with elevated aldosterone production
  • Hypotension with hyperkalemia
  • Female will show lack of secondary sex characteristics
  • Male will have pseudohermaphroditism
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33
Q

21 Deficency

A
  • Will have loss of aldosterone, 11-DOC, and cortisol
  • Hypotension, hyperkalemia and masculinization
  • Females will show pseudohermaphroditism
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34
Q

11 Deficency

A
  • Will have loss of aldosterone and cortisol with incerase in sex and 11-DOC
  • Leads to HTN (11-DOC) and masculinization
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35
Q

Growth Factor Receptors

A

JAK-STAT

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36
Q

IP3

A

GHRH, Oxy, GnRH, TRH

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37
Q

Cortisol

A
  • Zona fasiculatis
  • Increased with ACTH
  • Causes: Increased alpha 1 expression, hyperglycemia, inhibits fibroblasts, decreases bone mineral density, inhibits immune response (loss IL-2 and apoptosis)
  • Lipocortin inhibits PLA-2
  • Carried on CBG, glucuronidation leads to renal excreition, can be measured with 24 hr cortisol in urine.
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38
Q

PTH

A

Released from Parathyroid chief cells

  • Causes increase in serum Ca and loss of phosphorus
  • Increases bone resoprtion (stimulate RANK-L on blasts, also stimualte m-CSF to increase clasts (monocyte lineage)
  • Increase 1 alpha hydroxylase in kidney to increase vitamin D active form
  • Increase renal loss of phosphorus and increase renal absorption of Ca
  • Stimualted by decrease in Ca and Mg
  • Inhibited by massive decrease in Mg (diuretics, alcohol, diahrrea)
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39
Q

Vitamin D (Cholecalciferol)

A
  • Produced in skin from cholesterol by UVB as D3 and dietary as D2
  • Sent to liver where converted to 25-OH form that is active storage form.
  • Kidney will metabolize with 1-alpha hydroxylase to active 1,25 form.
  • 25,24 form is inactiv
  • Funtions to increase Ca and Phosphate resportion in gut.
  • Production stimulated by low levels of Ca and P
  • Deficency in childhood leads to rickets and osteomalacia in adults
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40
Q

Calcitonin

A
  • Causes decreased bone resportion and increased bone deposition of Ca leading to decreaesed levels of blood Ca
  • Stimulated by elevated Ca
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41
Q

NO

A

cGMP signalling Mechanis

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42
Q

ANP

A

cGMP signalling mechanism

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43
Q

Releasing hormones besides CRH

A

IP3 signalling mechanism

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44
Q

ADH V1 and Oxytocin

A

IP3

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45
Q

Ang 2

A

IP3

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46
Q

Growth Factors

A

RTK and MAPK

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47
Q

PRL and GH

A

JAK/STAT receptor associate TK

48
Q

Cytokines

A

JAK/STAT

49
Q

Steroid Horomone Binding Globulins

A
  • Increasd by estrogens (OC and pregnancy)
  • Decreased by androgens
  • Sequester steroid homones and decrease effective concentration
  • Also decreasd with cirrhosis
50
Q

Thyroid Hormone Physiologic Functions

A
  • T3 is more active than T4, peripheral 5’ deiodinase
  • Increase B1 receptors (Heart function increased)
  • Inrease BMR through increase Na/K ATPase
  • Cause hyperglycemia (increase glucose production)
  • Necessary for bone and brain development (cretinism)
51
Q

Thyroid Hormone regulatio

A
  • TRH from hypothalamus increases PRL and TSH release
  • TSH stimulates T3/T4 release increase thyroid peroxidase activity
  • Free T3 causes decreased sensitvity to TRH at level of AP
52
Q

Thyroid Hormone Production

A
  • Thyroid peroxidase perfoms oxidation, organification, and coupling of iodone to thyroglobulin (tyrosine)
  • T4 is main secreted hormone, changes to T3 peripherally with 5’ deiodinase, T3 binds Receptor tighter
53
Q

Wolf Chiakoff Effect

A

-Elevated iodine causes a transient decrease in thyroid production

54
Q

Propylthiouracil

A

-Causes decrease in thyroid peroxidase activity and decrease in peripheral function of 5’ deiodinase

55
Q

Methimazole

A

-Inhibits thyroid peroxidase

56
Q

Cushings Syndome Symptoms

A
  • Weakness, used for GNG
  • Striae-Coristol inhibits fibroblasts
  • HTN: Induce alpha 1 receptors
  • Osteoporosis
  • Immunosupression: (Apoptosis, decerase IL-2, decrease histamine, block PLA-2)
  • Fat deposits
  • Hyperglycemia
  • Amenorrhea
57
Q

-Cushings Causes

A
  • Iatrogenic: Leads to bulateral atrophy of adrenal glands
  • Tumor or hyperplasia of adrenal gland leading to unilateral enlargment and unilateral atrophy
  • ACTH tumor (Cushings disease) Bilateral hyperplasia of adrenals. Cortisol will be supressed with high dose dexamethasone supression
  • ACTH tumor paraneoplastic: No supression. Most commonly Lung (small cell or bronchial carcinoid)
58
Q

Cushing Dx

A
  • Symptoms

- ELevated 24 hr urine with glucuronidated cortisol

59
Q

Primary Chronic Hypoaldosteronism (Addisons)

A
  • Decreased aldosterone, and cortisol from adrenal hypoplasia
  • Most commonly autoimmune, can be TB and also metastasis from lungs
  • Adrenoleukodystrophy also
  • Symps: Hypotension, Hyponatremia, Hyperkalemia, Acidosis. Skin hyperpigmentation from POMC
60
Q

Secondary Chronic Hyperaldosteronism

A
  • Decreae pituitary ACTH: Tumor

- Same symptoms without skin changes

61
Q

Acute adrenal insuficcency

A
  • Nisseria Meningitidis causes waterhouse freidrichson or acute hemorrhagic infarction of adrenals bilaterally
  • DIC and loss of cortisol often fatal
62
Q

Primary Hyperaldosteronism (Conn’s)

A
  • Caused by tumor or hyperplasia of adrenals.
  • Leads to hypertension, Hypernatremia, Hypokalemia, Alkalosis.
  • Renin levels will be low
  • Tx: Surgery and spironolactone
63
Q

Secondary Hyperaldosteronism

A
  • Elevations in RAS lead to hyperaldosterone.
  • Same symtoms with an elevated Renin
  • Renal artery stenosis, fibromuscular dysplasia, atherosclerois, CHF, anything that will lead to decreased renal perfussion.
  • Ang II activates aldosterone synthase
  • Tx: Spironolactone
64
Q

Adrenal Crisis

A
  • Hypotension and volume contraction due to adrenal failure

- Can be caused when steroid therapy is rapidly removed because of adrenal atrophy that has occured.

65
Q

Pheochromocytoma

A
  • Tumor of the adrenal medulla. NC cells that are S-100 +
  • Recieve input from primary sympathetics with Ach the NT
  • Release of Epi, Norepi, and Dopamine leads to episodic HTN, palpitations, heacache and SANS signs (Skin pallor)
  • Dx with elevated serum metanephrines and elevated urinary VMA, product of MAO metabolism. (HVA more specific for neuroblastoma in kids)
  • MIBG scan can show ectopic locations, commonly bladder
  • Associated with: NF-1 (AD oncongene), VHL, MEN2 (medullary thyroid and pheo are necessary, RET)
  • Tx: Alpha and beta blockade. Surgery must be performed after administration of phenoxybenzamine
66
Q

Caetacholamine synthesis

A
  • Phenylalanine to tyrosine (phenylalanine hydroxylase)
  • Tyrosine to L-DOPA (THB and tyrosine hydroxylase)
  • L-DOPA to Dopamine (B6, Dopa decarboxylase)
  • Dopamine to Noreip (Vitamin C, Dopamine decarboxylase)
  • Norepi to Epi (SAM, Phenylethanolamine-N-Methyl Transferase)
67
Q

THB

A
  • Deficency will cause atypical phenylketonuria
  • Impaired caetacholamine synthesis and NO metabolism
  • Made from GTP endogenously
68
Q

Neuroblastoma

A
  • Most common extraranial mass in kids.
  • Most often presenst as abdominal mass, and is less likely associated with HTN
  • Leaks dopamine, Nor/epi, test urinary HVA
  • Localize with MBIG scan, most commonly in adrenal medulla but can be other places
  • Overexpression of N-Myc
  • Associated with NF-1 and Beckwith-Wiederman
69
Q

Hypothyroid Clinical Manifestations

A
  • Cold intolerance, bradychardia, diastolic HTN, Constipation, slowed reflexes, depression
  • Facial and periorbital myxedema
  • Hypercholesteroemia and hypoglycemia
  • Yellowing of skin because T3/4 necessary for beta carotene metabolism
  • May cause elevations in TRH leading to increased PRL and oligo or amenorrhea
70
Q

Myxedema Coma

A

Decompensated hypothyroidism generally brought on by stress.

  • Severe hypotension, bradychardia, resp depression and decreased temp
  • Treat with thyroid, cortisol, warming.
71
Q

Hashimotos

A
  • Auto antibodies to thyroglobulin or thyroid peroxudase. Associated with HLA-DR5
  • May present early as hyperthyroid but eventually becomes hypothyroid
  • Moderately enlarged and nontender thyroid
  • Lymphocytic infiltrate with germinal centers that predispose to marginal zone lymphoma
  • Hurthle cells, large eosionphilic cells around colloid
72
Q

Cretinism

A
  • Congenital and perinatal severe insufficency of thyroid
  • Most commonly because of iodine deficency and endemic goiter, but is rarely caused by congenital thyroid structural or funcional mutations
  • Retardation and decreased stature. Born with large tongue, large belly, and omphalocele/umbilical hernia
  • Retardation because thyroid is necessary for synapse formation and also for bone growth
73
Q

Dequarvians subacute thyroiditis

A
  • Granulomatous inflammation (type 4) following viral illness
  • Thyroid status may be hyper/hypo/eu
  • Painful goiter! with elevated ESR and associated jaw pain
  • Self limited
74
Q

Ridels Thyroiditis

A
  • Fibrous replacement of thyroid tissue. Thought to be related to IgG4 systemic fibrosing diseases
  • Will cause hypothyroidism signs and a rock hard painless thyroid
  • Often has extension into the local laryngeal structures possibly compromising speaking and breathing.
  • Differntiate from anaplastic carcinoma, occurs mainly in younger females.
75
Q

Goiter

A

Most common cause is goiter which is caused by a lack of iodine leading to impaired thyroid production causing and increase in TSH which is trophic for the thyroid
-Increased ratio of free T3/T4

76
Q

Toxic Multinodular Goiter

A
  • Idiopathic focal hyperplasia of thyroid nodules. Will present with a non uniformal enlargment and hyperthyroidism.
  • Accumulated mutation in TSH gene that causes TSH independent production
  • Can detect hot nodules with RIA. Cancer is hypothyroid and will be cold on RIA
77
Q

Jon Basedow phenomenon

A

-Patients with long term iodine deficency and goiter may become hyperthyroid after replacement of iodine because of hyperplasia

78
Q

Graves Disease

A
  • TH2 hypersensitivity with TSI autoantibodies to TSH receptor leading to hyperthyroidism
  • Diffuse nontender goiter that will show enlarged follicles with colloid scalloping on histology
  • Will show pretibial myxedema because TSI stimulates fibroblasts
  • Tx: Methimazole and PTU
79
Q

Hyperthyroidism

A
  • Increase in BMR due to increased Na/K ATPase activity
  • Increase in B1 expression and subsequent hypersensitivity to caetacholamines
  • Pretibial myxedema (graves, TSI)
  • Arrythmias, tachychardia, hypocholesterolemia, hyperglycemia
  • Diahrrea
  • Staring gaze because of SANS activation of levator palpebrae superioris
  • Labs will show elevations in T3 and T4 with reductions in TSH. May also show elevated ALP because of increased bone turnover
80
Q

Thyroid Storm

A
  • Extreme increase in thyroid production and serious consequences.
  • Generally arises in the context of stress because of elevations in caetacholamine release
  • Death most likely by arrythmia
  • Treat with beta blockers, iodine (wolff-Chiackoff) and PTU (5’deiodinase)
  • Increased ALP often seen
81
Q

Thyroid cancer

A

Generally focal enlargment, not diffuse

  • generally non functional and will be cold on RAI
  • If treated with T3/T4 before surgery there will be decrease in TSH and shinkage of gland for easier surgery
82
Q

Papillary Carcinoma

A
  • Most common type of carcinoma greater than 80%
  • Linked to early exposure to radiation (acne irradiation)
  • Focal enlargment
  • FNA will show cells with pale nuclei (orphan annie) and nuclear grooves
  • Will also show psammoma bodies (papillary carcinoma)
83
Q

Follicular Carcinoma

A
  • 2nd most common cause and can be adenoma or carcinoma
  • Encased by fibrous sheath, and is ademona if not through sheath and carcinoma if it is.
  • Spreads hematogenously (RCC, HCC, Choriocarcinoma also)
84
Q

Medullary Thyroid Carcinoma

A
  • Carcinoma of parafollicular C cells that secrete calcitonin
  • Tumor cells in an amyloid stroma. Amyloid from calcitonin secretion
  • Seen in all cases of MEN2 A and B. Also both have pheo.
  • 2A: parathyroid
  • 2B: Neruofibromas
85
Q

Anaplastic

A
  • Highly malignant and seen most comonly in elderly
  • Poorly differentiated spindle cells
  • Hard shrunken thyroid that often invades local structures causing breathing problems or speaking problems.
  • Differentiate from riedels mainly on age of patient
86
Q

Marginal Zone B Cell Lymphoma

A

-Seen in Hashimotos thyroiditis where germinal centers form in thyroid and give rise to marginal zone lymphomas.

87
Q

Primary Hyperparathyroidism

A

Most commonly and adenoma, but can also be carcinoma (MEN2)

  • Elevations in PTH lead to hypercalcemia and hypophosphatemia.
  • PTH only responds to free Ca (not complexed with albumin or phosphate)
  • PTH activates Osteoblasts to express RANK-L to activate osteoclasts
  • Increased ALP, bone pain, constipation, Renal stones, dystrophic calcification (nephrocalcinosis)
  • cAMP urine test, PTHR is Gs which means stimulation will cause elevations in urinary cAMP
  • Siezures and weakness
  • Polyuria
  • Cardiac Arrest!
88
Q

Secondary HyperPTH

A
  • Most often caused by renal failure that leads to calcium wasting, phosphate retention, and inability to produce vitamin D
  • Low Ca with High PTH
  • Phosphate will also be raised which will further decrease free Ca
89
Q

3 hyperPTH

A
  • End organ resistance to PTH or autonomous PTH secretion from PTH gland
  • Generally occurs in the context of renal disease
  • Elevations in PTH and elevations in Ca
90
Q

Osteitis Fibrosa Cystica

A

Elevations in PTH will cause increased bone destruction and replacement with fibrous tissue.

  • This can cause bone pain
  • Most commonly associated with primary hyperPTH
91
Q

Renal Osteodystrophy

A

-Renal failure that lead to increased PTH that causes excessive bone breakdown.

92
Q

HypoPTH

A
  • Most commonly caused by surgica error
  • Digeorge, autoimmune distruction
  • Presents with hypocalcemia and not increase in PTH
  • Muscle spasm and perioral tingling
93
Q

Pseudohypoparathyroidism

A
  • Congenital malfunction in Gs portion of PTH receptor that leads to renal non-responsiveness
  • Short stature and shortened 4th and 5th digets in the context of elevated PTH and decreased Ca
94
Q

PTHrP

A
  • Paraneoplastic syndrome that causes incerases in Ca
  • most commonly breast and squamous cell lung
  • Ca is also often increased in cancer for other reasons.
95
Q

Pituitary Adenoma

A

Most commonly nonfunctional causing mass effect: Headache, panhypopit, bitemporal hemianopsia

96
Q

Prolactinoma

A
  • Most common functional of pituitary
  • Causes galactorrhea and amenorrhea in women and decreased libido and decreased sperm in men (inhibit GnRH)
  • Tx with pergolide or bormocriptine
  • Can be mimicked by antipsychotics (dopamine antagonists)
97
Q

GHoma

A

Second most common

  • Acromegally in adults and gigantism in kids
  • Increased IGF-1, also will not respond to glucose supression test
  • Hyperglycemia and organomegally
  • most common cause of death is cardiomegally and CHF
  • Treatment with resection or octreotide
98
Q

Diabetes Insipidus

A
  • Impaired signalling and fuction of ADH leading to increased urine output, polydypsia and hyperoslmolarity
  • ADH works on collecting ducts and distal tubule late
99
Q

Central DI

A
  • Decreased ADH production
  • Will improve with Desmopressin administration
  • Caused: Tumor (craniopharyngoma, Trauma, histiocytosis)
100
Q

Nephrogenic DI

A
  • Kidney doesn’t respond to ADH
  • Doesn’t improve with desmopressin
  • Commonly caused by Lithium (Tx amiloride), congenital
  • Tx: Hydrocholorothiazide, indomethacin, both decrease renal perfusion , decreased GFR increase retention
101
Q

SIADH

A
  • Elevated secretion of ADH leading to hypervolemia and dilutional hyponatremia
  • Can present with mental status changes and siezures
  • Caused by lung pathology: Small cell carcinoma, Legionella, COPD
  • Caused by drugs: Cyclophosphamide, Trauma
  • Correct Na slowly
  • Treat with conivaptan or demeclocycline to block ADH.
102
Q

Craniopharyngoma

A

-Tumor of rathkes pouch that can cause hypopituitarism

103
Q

Sheehan’s Syndrome

A
  • Growth of AP during pregnancy and hypotensive causing blood loss during birth leads to infarcion
  • Presents as inability to breast feed
104
Q

Empty Sella

A
  • Absence of sella due to herniation of arachnoid or brain matter and compression
  • Most commonly seen in obese women
  • MRI will show no AP in sella
105
Q

Diabetes Mellitus I

A
  • Caused by immune destruction of beta cells (central in islets of langerhans). Ab present and also type 4 hypersensitivity. Will show leukocytic infiltrate
  • Minimal genetic concirdance when compared to type 2
  • DKA risk
  • Insulin dependent
106
Q

Diabete Mellitus 2

A
  • Caused by reduced sensitivity to insulin peripherally. Decrease receptor and downstream signalling
  • High genetic concordance 90% in identical twins
  • Highly associated with obesity
  • NonKetoticHyperosmolar Coma is risk
  • Amylin deposits of insulin amyloid will be seen in islets
107
Q

DKA

A
  • Elevations in serum ketones (Beta hydroxybutyrate more than acetone) leading to high anion gap metabolic acidosis
  • Often caused by stress which induces cortisol and increased FFA breakdown
  • Present with metabolic acidosis, serum hyperkalemia with cellular hypokalemia (transcellular shift to buffer pH)
  • Kussmaul respiration, epigastric pain with vommiting and naseua
  • Can cause mucor, cardiac arrythmias, cerebral edema, candida infection
  • Tx: Glucose and insulin. Also K to replete the intracellular stores
108
Q

NonKetotic Hyperosmolar Coma

A
  • Massive elevations in blood glucose lead to severe polyuria and dehydration causing electrolye imbalances with hyperosmalrity possibly progressing to coma
  • Commonly caused by stress which induces release of epi and GH leading to GNG stimulation and glycogenolysis
  • Tx: Fluids, Electrolytes, insulin
109
Q

Non enzymatic glycosylation

A
  • Glucose exists in open and closed form, open is highly reactive and can glycosylate basement membrane
  • Small vessel leads to hyaline arteriolosclerosis, microalbuniuria progressing to nephrotic syndrome (nodular sclerosing with kimmeslstein wilson nodules), glaucoma, retinopathy
110
Q

Osmotic Damage

A
  • Elevated glucose turned into sorbitol by aldose reductase which cannot leak out of tissue and builds up causing increased pressure.
  • Most commonly seen in tissues that can take up glucose independent of insulin
  • Lens causes cataracts
  • Schwann Cells causes peripheral neuropathy
  • Pericytes cause retinal hemorrhage
111
Q

Complications of pregnancy and diabetes

A
  • Human placental lactogen acts simliar to GH and can cause elevations in glucose levels
  • Listed complications more associated with DM than Gestational diabetes
  • Most common cause of transposition of the great vessels
  • Caudal regression syndrome: Sacral agenesis
  • PDA, polydactyly, aortic coarcataion, hypospadias
112
Q

Carcinoid

A
  • Neuroendocrine tumor that secretes large amounts of seretonin
  • Most common tumor of small bowel and appendix, but will be assymptomatic due to first pass metabolism unless metastasize (most commonly to liver)
  • Elevated levels of urinary 5-HIAA (5-HT metabolite)
  • Can also be from neuroendocrine tumors in lung
  • Causes diahrhrea, flushing, asthma, right sided valvular problems.
  • Niacin wasting because of cofactor requirment
  • Tx: octreotide
113
Q

Zollinger Ellison

A
  • Gastrin secreting tumor, most commonly of pancreas (MEN-1) but can also be from small bowel
  • Causes parietal cell hyperplasia and treatment resistant gastric ulcers that may extend into jejunum
  • Tx: Somatostatin, PPI
114
Q

MEN-1

A
  • AD mutation in TSG leads to tumors in the pancreas, pituitary, and parathyroid
  • Gastrinoma: ZE
  • VIPoma: Diahrrea and hypokalemia
  • Insulinoma: hypoglycemia with C peptide
  • Glucagonoma: hyperglycemia with painful itchy rash
115
Q

MEN2A

A

-Mutation in RET oncogene causes Medullary Thyroid, Pheochromocytoma, PTH

116
Q

MEN2B

A
  • Muation in RET oncogene leads to Medullary Thyroid, Phoechromocytoma, and Cutaneous or GI neruotumors
  • Also causes marfanoid habitus

Boards Path (20 decks)

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