Endocrine Flashcards
(197 cards)
1
Q
What 4 things do you think of when it comes to hyperthyroidism
A
Graves
Medication cause = Amiodarone
Multi nodular goiter
Toxic thyroid adenoma
2
Q
What does the thyroid look like with Graves’ disease
A
Diffuse non tender enlargement
3
Q
What does the thyroid look like in multi nodular toxic goiter
A
Bumpy irregular asymmetric with nodules
4
Q
4 general sxs for hyperthyroidism
A
Dysrhythmia
Moist Pretibial myxedema
Increased DTRs
Proptosis
5
Q
Lab findings and antibodies in hyperthyroidism
A
Low , NML TSH ; high FT4 or FT3
Thyroid stimulating immunoglobulins
6
Q
What two things do you think of with high FT4/FT3 labs and low radio iodine uptake
A
Subacute thyroiditis and Amiodarone exposure
7
Q
Give 4 talking points for hyperthyroid medications
A
First and Best = Radio Iodine ablation ; common in Graves’ disease
Methimazole ; can be used if they dont want ablation
PTU = best in pregnancy
Propanolol best for hyper sympathetic sxs
surgery if large goiters and contraindications
8
Q
What is the #1 risk factor for a thyroid storm?
A
1 infection
9
Q
What are three complications to think of in thyroid storm?
A
Heart failure
Hyprecalcemia
Osteoporosis
10
Q
Which hyperthyroid medication is teratogenic
A
Methimazole
11
Q
How does exogenous iodine effect thyroid hormone?
A
Inhibits release of thyroid hormone
Used days [7] before thyroidectomy
12
Q
What do yo have to remember when administering iodine
A
Block the sympathetic pathway first with PTU or Methimazole (1hr before)
13
Q
What is the benefit of steroids in thyroid storm
A
Can treat adrenal insufficiency and autoimmune process in Graves’ disease
14
Q
What are the main antibodies in hypothyroidism (Hashimotos)
A
Anti TPO and anti thyroglobulin
15
Q
What 4 medications can cause hypothyroidism
A
Methimazole
PTU
Lithium
Amiodarone
16
Q
What are two uncommon sxs of hypothyroidism
A
Slow mentation
Menorrhagia
17
Q
What’s the effect on DTRs in hypothyroidism
A
Delayed!
18
Q
What is the extreme/severe version of hypothyroidism
A
Myxedema coma
19
Q
What is the dose adjustment per levels of thyroid hormone (TSH) ?
Less the 5-10
10
Less than 20
A
Less the 5-10 = 25 to 50
10 = 50 to 75
Less than 20 = 75 to 100
20
Q
What it the #1 cause of supparative thyroiditis
A
Staph A.
21
Q
What proceeds subacute thyroiditis normally?
A
URI
22
Q
What is the tell tale sign of subacute thyroiditis
A
The gland itself is painful ; low grade fever ; pain that radiates to the ears
23
Q
What are the tell tale signs of bacterial thyroiditis
A
Severely tender thyroid ; sudden onset fever erythema and fluctuation
24
Q
What studies would you get with subacute thyroiditis or infectious
A
Subacute
> radio iodine uptake = LOW
Infectious
>thyroid U/S
>FNA with gram stain
25
Do you give antibiotics to subacute thyroiditis?
NO
ASA/ NSAIDS
Prednisone
Supportive care
26
Physical exam findings in thyroid nodules (3)
Smooth firm
Well outlined
Painless
27
For a thyroid nodule that has low TSH what should you do?
Radionuclide thyroid scan
HOT = benign
COLD = MALIGNANT
28
For a thyroid nodule that has normal to high TSH what should you do?
Thyroid U/S
29
What are malignant findings for thyroid on U/S
Hypoechoic with irregular margins and micro calcifications
30
If a thyroid nodule is suspicious for malignancy on U/S what do you do?
FNA
31
If a thyroid nodule is causing dysphagia and proved benign what can you do for management? If what?
RF ablation if greater than 3cm
32
What is the monitor time for thyroid nodules
6 months by U/S and then yearly
33
Most common type of thyroid cancer
Papillary carcinoma
34
Talking points for medullary thyroid cancer (2)
Arises from parafollicular cells
Produces calcitonin
35
Talking point for follicular thyroid cancer
Higher rates of metastasis
36
What do you need to know about anaplastic carcinoma
Common in elderly MOST AGGRESSIVE
37
What are secondary findings associated with medullary thyroid cancer
Diarrhea
Flushing
38
What are secondary findings associated with anaplastic thyroid cancer
Dysphagia
Laryngeal nerve involvement
Hoarseness
39
Metastatic papillary and follicular cancers often have an increase in what hormone?
Serum thyroglobulin
40
What is the management for thyroid cancer (papillary and follicular)
Total thyroidectomy
41
What is the #1 cause of primary hyperparathyroidism
Parathyroid adenoma
2nd = lithium use or malignancy
42
2 common reasons for secondary hyperparathyriodism
CKD causing low calcitriol ; which causes increased PTH
Vitamin D deficiency
At worst think ESRD and Renal transplant
43
Dont forget what sxs with hyperparathyriodism and why
Stones Moans Groans and Psych Overtones
Think: Hypercalcemia
44
3 management things to remember in severe Hypercalcemia
IVF
Furosemide
Bisphosphonates and Calcitonin
45
If someone has hyperparathyriodism secondary to CKD you will likely replace what deficiency?
Calcitriol
46
Severe Hypercalcemia can be treated with
Cinacalcet
47
What deficiency can cause hypoparathyroidism
Magnesium deficiency
48
What should you think of with hypoparathyroidism or low calcium
Chovsteks
Trousseau’s sign
Increased DTRs
Low PTH Low Ca INCREASED PHOSPHATE
49
3 etiologies of adrenal insufficiency
Infection [TB, Fungal, HIV]
Destruction [Autoimmune]
Deficiency [Autoimmune]
50
Difference between primary and secondary adrenal insufficiency
Primary = low cortisol, Low DHEA, Low Aldosterone ; because the adrenal gland is not able to read the ACTH; so an increaed ACTH which results because of high CRH [adrenal gland tumor/infection]
Secondary = low cortisol, Low DHEA, Normal Aldosterone ; because the pituitary gland is sending a low ACTH signal and a high CRH signal results to try to fight the low ACTH [pituitary tumor]
Tertiary is a problem of the hypothalamus
51
How do we treat adrenal insufficiency
Primary = hydrocortisone / prednisone + fludrocortisone [corrects the low aldosterone]
52
What is ACTH independent Cushings?
Overproduction or overconsumption of steriods
[independent of your own ACTH]
53
What is ACTH dependent Cushings?
Cushings Disease !
Due to : pituitary tumor or ectopic ACTH production
54
What are the main 3 tests we want to do for Cushings
Dexamethasone suppression test
24 hour urinary free cortisol
ACTH level testing
55
What is a positive dexamethasone suppression test? Also talk about ACTH and disease vs. syndrome
Above 1.4 mL allows you to know that the cortisol can not be suppressed by dexamethasone.
ACTH will be low in Cushings Syndrome
ACTH will be high in Cushings Disease
56
A positive 24 hr urinary free cortisol will have what ?
High levels of cortisol in the AM = positive test
57
What is another name for hyperaldosteronism
Conn Disease
58
3 clinical features of conn disease
Headache
Metabolic alkalosis
Weakness
59
What it is the concern with acute increased SIADH
Cerebral edema
60
What are lab findings in SIADH (3)
Low serum sodium
Low serum osmolality
Increased urine osmolality
61
What are the lab findings of diabetes insipidous
Incr serum sodium
Incr serum osmolality
Dec urine osmolality
62
4 interventions for SIADH
Water restriction to 500-1500 mL per day
Correct sodium [no more than 10 mEq in 24 hrs // 18 mEq in 48 hrs]
Vasopressin = VAPTANS
Loop diuretic
63
3 main complications of SIADH
Seizures
Osmotic Demylenation Syndrome [SHRINKING OF THE BRAIN]
Coma/death
64
Diabetes Insipidous think what?
Low or Resistance to ADH
Large amounts of Dilute Urine
65
Explain Central vs. Nephrogenic DI
Central = Idio; Trauma; Surgery; Malignancy // ADH is not PRODUCED at the pituitary
Nephrogenic = Genetics[KIDS] Medications[Lithium] , CKD // ADH is not RECOGNIZED at the renal tubule
66
Lab studies for diagnosis of DI
Low osmolality // Low specific gravity urine
High serum osmolality
High NA+
Water deprivation test positive
67
What is the water depreciation test in DI
Still pee large amounts of DILUTE urine
-Showing that there is no increased in ADH production to decrease urine production and osmolality
68
What imaging should i get if I suspect central DI
Brain MRI
69
What happens when DI patient is given desmopressin? Central vs. Nephro
Central = increase in urine osmolality
Nephro = minimal or no increase in urine osmolality
70
Management for central DI
Desmopressin = INTRANASAL
Thiazide , Carbamazepine , Chlorpropamide
71
Management for nephro DI?
Low solute diet
Thiazide diuretic
NSAIDS
If continuing lithium use => Amiloride
72
How are pituitary Adenomas classified
Secretory and Non Secretory
73
What are the 4 types of secretary pituitary adenomas
Prolactinoma
Somatotropinoma
Corticotroph adenoma
Thyrotropinoma
74
3 sxs significant in macro Adenoma of the PT gland > 1cm
Bitemporal heminopsia
Headache
Diplopia
75
3 talking points for somatotropinoma
Adults = acromegaly
Kids = gigantism
Often HYPERglycemic
76
Corticotropinoma sxs (3)
Weight gain
Hypertension
Proximal muscle weakness
77
What are labs for somatotropinoma
Increased IGF-1 ; abnormal glucose tol testing PO
78
Imaging of choice for pituitary adenoma
MRI with contrast
79
Imaging of choice for pituitary adenoma
MRI with Contrast
80
What guides management in pituitary Adenoma resection
Symptomatic or not?
81
How do we treat prolactinoma
Not resection
Dopamine agonist =Cabergoline and Bromocrpitine
82
Treatment of somatropinoma
First give octreotide, an analog of somatostatin
Then surgery or for residual disease
83
Diabetes type 1 is
Autoimmune destruction of pancreatic B cells = decrease in insulin production
84
When is the peak incidence of DM1
Age 4-6 and 10-14 years old
85
What is the reason for Kussmauls breathing in DKA
Respiratory response to metabolic acidosis
86
Diagnosis of DM [4 examples]
Fasting plasma glucose over 126 on 2 occasions
Random glucose higher 200
2hr OGTT over 200
HbA1c over 6.5 %
87
3 lab indications of DKA
High anion gap
Sodium bicarbonate over 18!
Ketonuria
88
Management of DKA
First reverse causes [infection]
IVF NML saline 0.9% until glucose = 250 ; then change to a 5% dextrose containing solution
Use KCL if necassary to correct Hypokalemia
Correct other electrolytes
89
How do we check for kidney disease in DM patients
Urine albumin : CREATINE ratio
Annually
90
When should you screen for diabetic neuropathy in type 1
3-5 years after diagnosis
91
Type 2 DM summary
Insulin resistance in tissues // decreased insulin release
92
What dietary patterns lead to risk for T2DM
Red meat
Processed meat
Sugar and sweetened beverages
93
What is pH normally in HHS
Over 7.3 [not acidotic-not dka]
94
Serum osmolality and bicarbonate in HHS
SO = over 320
Bicarbonate = over 15
95
Screening for T2DM
Any age with BMI over 25 and one risk factor
Or at age 35-70 yrs old ; and if normal every 3 years after that
96
4 risk factors to remember in T2DM
HTN greater 140/90
HDL less than 35 Triglycerides over 250
History of PCOS
Physical inactivity
97
Anterior lobe description of the hypothalamus
Hormones first made here
Sent through portal veins
To increase anterior pituitary hormone production
—> target organs
98
Posterior lobe description of hypothalamus
Hormones made here then sent via :
Neurons —> posterior pituitary
Hormones —> target organs
99
Somatotrophs secrete what hormone
GH —> liver adipose
IGF hormone increased =
Growth of muscle bone
100
Lactotrophs secrete what
PRL —> targets mammary glands
—> milk production
101
corticotroph secretes what hormone
ACTH —> targets adrenal cortex
Adrenal release of cortisol —> aldosterone —> androgens
= increase in glucose and fluid volume
102
Thyrtroph release what hormone
TSH —> thyroid —> thyroxine and triiodothyronine
=regulation of metabolism
103
Gonadotroph releases what hormone
FSH / LH —> gonads
Gonads release —> estrogen and progesterone and testosterone
=egg sperm production // ovulation
104
ADH comes from where and causes what
Kidneys
= increase water absorption
105
Oxytocin is produced in what organs and does what
Uterus ; mammary ; male reproductive tract
= contraction for delivery lactations ; sperm release
106
Micro vs. Macro adenoma of pituitary
Less than 10 = micro
Over 10 = macro
107
What CN is impacted by pituitary adenoma
CN2 @ the optic chiasm
= Bitemporal; hemeniopsia
And opthalmoplegia = CN 346
108
Best imaging study for pituitary adenoma
MRI with contrast
109
MC cause of hypopituitarism
Pituitary adenoma
110
ACTH deficiency think
Addisons
111
Klinefelters =
LH and FSH receptor mutations
112
Turners =
Ovarian (primary) hypergonadotropic
113
2 exogenous causes of secondary hypogonadism
Spirnolactone
Steriods
114
When should you test estrogen or testosterone
8 am - Morning
115
Central vs. Peripheral gonadism
Central = hypo = low normal FSH/LH
Peripheral = hyper = high FSH and LH
116
Even if T is low you should not give testosterone to what population
Prostate cancer pts
Monitor hematocrit
117
How do you treat infertility in hypogonadism
Gonadotropin
118
Prolactinoma diagnosis
MRI with gadolinium
119
Prolactinoma levels of prolactin and TXM
Over 200 NG/mL
TXM = dopamine agonist —> cabergoline or bromocriptine
120
4 other causes of hyeprprolactinoma
Atypical antipsychotics
Pregnancy
Stalk compression
Hypothyroidism
121
Prolactin deficiency =
Sheehans syndrome —> delivery
= lack of lactation at delivery and drop in blood pressure —> post partum hemorrhage
122
Best screening test for GH excess =
IGF -1 will be HIGH
123
GH excess treatment
Trnassphneoidal surgery
Dop agonist = cabergoline
Somatostatin = octreotide
GH receptor antagonist
124
TXM GH deficiency
Recombinant human GH
Correct metabolic issues
Treat to nml IGF-1 level
125
Being on GH can make you at risk for
Psuedotumor cerebrii
126
TXM SIADH
Fluid restriction
Furosemide
Treat the cause
127
Central vs. Nephrogenic DI
Central = decreased pituitary secretion of ADH
-etiology : HEAD TRAUMA
Nephro = decreased response to ADH in kidneys
-etiology: drug induced
128
Drugs that can cause Nephro DI
Lithium
Colchicine
Amphotericin B
Gentamicin
129
Condition that can cause nephrogenic DI
Hypercalcemia
130
Does nephrogenic DI respond to desmopresin ?
NO
*but central does
131
Too much desmopressin can equal
Hyponatremia
132
3 systemic effects of GC release from adrenal cortex
Increase plasma glucose levels
Mx vascular integrity
Decrease inflammation
133
Adrenal medulla produces
Catecholamines
134
Cortex of adrenal gland
-Glomerulosa
-Fasciculata
-Reticularis
G = mineralcorticoid
F = GC
R - androgens
135
4 causes of pseudo Cushings
Alcoholism, Pregnancy , Anorexia , Depression
136
Cortisol and
ACTH are high when
In the morning
137
Overnight dexamethosaone suppression = low cortisol think
Suppressed by exogenous steriods
138
Nelson syndrome
Post pituitary r2
Recurrent severe enlargement of adenoma
139
Secondary adrenal insufficiency MC cause
Cessation of steroids
140
In secondary adrenal insufficiency aldosterone is
Intact
141
Skin in secondary adrenal insufficiency
Alabaster skin
142
Test for adrenal insufficiency
Consyntropin test
High = primary
Low = secondary
143
Androgen deficiency in adrenal insufficiency is treated by
DHEA
144
Adrenal crisis mgmt
Hydrocortisone high dose IV
Fluid // electrolyte correction
Broad spectrum ABX if dont know cause
145
Unilateral or bilateral adrenal hyperplasia txm
Spirinolactone
146
Muscle weakness ; paresthesia ; tetany ; headache ; polys
+
Refractory HTN
Think
Hypokalemia form primary aldosteronism
147
Pheo = rule of
10s
10% of everything
148
Beta blocker use in pheo
Used only after alpha to avoid worsening of HTN
149
Elevated serotonin tumor think
Carcinoid tumor ;
W/ ABD pain l wt loss ; glossitis
150
MEN inheritance
Autosomal dominant
151
MEN 2 think what 3
Pheo
Parathyroid
Medullary thyroid carcinoma
152
T4 and T3 need what in order to be released from the thyroid
Iodine + Thyroglobulin + Enzyme TPO
153
MC autoimmune hyperthyroidism in the US
Graves
154
Iodine deficiency think
Multi nodular goiter or Adenoma
155
Main medication that induces hyperthyroidism vs hypo
Hyper = Amiodarone
Hypo = Lithium
156
Arrythmia assoc with hyperthyroidism
A fib or SVT
157
Eye effects in Graves’ disease [4]
Infiltration opthlamopathy
Upper lid lag on downward gaze
Each eye can be affected differently
Worse with smoking
158
Thyroiditis is often
TRIPHASIC
Phases lasting up to a few months
159
Graves ab
Thyrotropin receptor antibodies
160
Subacute and infectious thyroiditis often has an elevated what
ESR
161
RAI uptake for the following :
Graves
Toxic multinodular goiter
Toxic adenoma
Subacute thyroiditis
Exogenous
G = diffuse symmetric uptake
T M G = patchy
TA = focal uptake
ST = low uptake
E = No uptake
162
Thyrotoxicosis acute mgmt
Beta blocker —> BMAE or propanolol [acute]
NSAIDs or Steriods —> thyroiditis [acute]
Mx = ATD
Methimazole = preferred
PTU = 1st trimester of pregnancy
163
RAI requires thyroid fxn to be what?
Euthyroid
164
Tachy delirious high fever N/V/D
Complication = from ?
= thyroid storm
From —> thyrotoxicosis
165
What is cretinism
Decreased mental and growth in infants and children
-hypothyroidism-
166
Congenital hypothyroidism presentation
Jaundice
Lethargy
Hoarse cry
Growth f.
Constipation
Hypotonia
167
Most increased cardio risk with what type of thyroid disease
Hypothyroidism
168
When are newborns screened for thyroid disease
First 2-5 days of birth
169
Hashimotos autoimmune ab
Anti-TPO and thyroglobulin ab
170
Hashimotos goiter described as
Diffusely heterogenous
171
Who gets a smaller vs. higher dose of Levothyroxine
Smaller = over age 60 or CAD
Higher = pregnancy
172
Hypothyroidism with cortisol insufficiency ; which do you treat first
Cortisol deficiency —> increased metabolic rate and set off and adrenal crisis
173
Myxedema crisis mgmt
IV thyroxine
Steriods
ICU admit
174
Workup for thyroid nodule
Exam finding —> get a TSH
TSH hot = benign
U/S if worrisome solid irregular calcified
Get TIRADS score
FNA —> for cytology and molecular testing
Monitored by : Bethesda system
175
Medullary thyroid cancer
Elevated calcitonin MEN flushing diarrhea
176
How does PTH affect
Renal tubule
Small intestine
Bone
Renal tubule —> increase Ca2+ absorption ; decrease phosphate absorption
Small intestine —> increase synthesis of vitamin D ; increase intestinal ca 2+ absorption
Bone —> formation and resorption for net effect
177
4 exogenous causes of hyperparathryroidism
Increase in PTH protein [cancer]
heme cancers
Sarcoidosis
Lithium thiazide diuretics
178
High PTH and high CA 2+ think
Bones
Stones
Groans
Moans
179
Arrhythmia assoc with hyperparathyroidism
Brady arrhythmia
180
Type 1 DM [4]
Complete destruction of pancreatic beta cells
Hyperglycemia
Acute onset sxs
DKA
181
Type 2 DM [4]
Peripheral insulin resistance
Decreased insulin response
Insidious ; Asian l Native American I AA I Latino
HHS
182
Bicarbonate in DKA vs. HHS
DKA = low
HHS = high
183
HHS onset
Days to weeks
184
Microvascular complications of DM
Retinopathy
Neuropathy
Nephropathy
185
Macovascular complications of DM
Coronary heart disease
Peripheral heart disease
Cerebrovascular diseae
“Chronic”
186
4 things to check in addition when suspect type 1
Positive ab
Low c peptide
Low insulin
Screen for thyroid and celiac disease
187
BMI over what gets DM testing
Over 25 or 23 in Asians
188
What type of diabetes gets annual diabetes tests
Annually for pre diabetics
189
NML DM testing should be retested when ; starting after age ___
3 year interval
After age 35
190
General goal for A1C in diabetics
A1C under 7%
Preprandial = 80-130
Postprandial = less than 180
191
Disadvantages to insulin
Weight gain
Hypoglycemia
192
Metformin can lead to what deficiency
B12
193
DPP4 has what two side effects
Pancreatitis
CHF
194
TZD meds side effects
Increases weight
CHF
Bladder Cancer
Bone fx
195
SU side effects
Hypoglycemia
Weight gain
196
What can help stabilize blood sugar after carbohydrate correction
Fat/Protein
197
Glucose less than 70 with AMS think about giving
Glucagon
