Clinical Flashcards
(102 cards)
1
Q
Major cause of severe hypercalcemia
A
Multiple myeloma
2
Q
Tx of severe hypercalcemia
A
Fist step is isotonic saline
100-200 cc/hr
3
Q
How can hypercalcemia present
A
Asymptomatically or very vague symptoms
Stones, bones, groans
4
Q
Which thyroid hormone is biologically active?
A
T3
5
Q
Primary hypothyroidism
A
Thyroid gland doesn’t make enough thyroid hormone
6
Q
Secondary hypothyroidism
A
Inadequate TSH from pituitary
7
Q
Tertiary hypothyroidism
A
Inadequate TRH from hypothalamus
8
Q
Congenital hypothyroidism
A
Cretinism
Brain damage, short stature
9
Q
Myxedema coma
A
Severe form of hypothyroidism
Often in undx pt exposed to stress
10
Q
Lab values of primary hypothyroidism
A
Elevated TSH
Low T3, T4
11
Q
Number one world wide cause of primary hypothyroidism
A
Iodine deficiency
12
Q
Number one US cause of primary hypothyroidism
A
Hashimoto’s
Thyroid peroxidase or thyroglobulin antibodies
13
Q
Subacute granulomatous thyroiditis
A
De Quervain’s thyroiditis
Painful
Preceded by viral illness - coxsackie and echo viruses
14
Q
Three phases of De Quervain’s thyroiditis
A
Initial hyperthyroidism from cytotoxic T cells damaging follicular cells and releasing T3, T4
Hypothyroidism until exhaustion of thyroid stores (weeks to months)
Euthyroid
15
Q
De Quervain’s Tx
A
NSAIDs
Steroids
16
Q
De Quervain’s Dx
A
Radioactive iodine uptake at 24 hours is LOW
17
Q
Post Partum Thyroiditis
A
anti TPO antibodies
Transient
2-10 months after delivery
Short course of LT4
18
Q
High yield drugs that cause primary hypothyroidism
A
Lithium, amiodarone
19
Q
Primary hyperthyroidism lab values
A
Decreased TSH
Increased T4
20
Q
Primary hypothyroidism lab values
A
Increased TSH
Decreased T4
21
Q
Central hyperthyroidism lab values
A
Increased TSH
Increased T4
22
Q
Central hypothyroidism lab values
A
Decreased TSH
Decreased T4
23
Q
Hypothyroid Tx
A
Levothyroixine (LT4)
Rx in pts with TSH of 4.5-10 mlU/mL with goiter or pts with TSH > 10 mlU/mL
24
Q
Myxedema coma tx
A
LT4 replacement
IV corticosteroids
25
Most common cause of hyperthyroidism in US
Graves Disease
26
Graves Disease
Autoimmune
Thyroid stimulating immunoglobins provide constant stimulation
Thyrotropin receptor is primary site of action
Excess lvls of T3, T4, and suppression of TSH
27
What is the hallmark of Graves Disease?
Exophthalmos (proptosis)
28
Graves Disease labs
```
Elevated T4, T3
Thyroperoxidase antibodies
Thyroglobulin antibodies
Thyroid stimulating immunoglobins (TSI) stimulation
Elevated radioactive uptake scan
```
29
What is diagnostic for Graves?
Thyroid stimulating immunoglobins (TSI)
30
What diagnostic modality is indicated in all pts with hyperthyroidism?
Ultrasound
31
Graves Tx
Antithyroid drugs - methimazole, propylthiouricil
Iodine 131
Surgery
High dose steroids for ophthalmopathy
32
Risk of what with antithyroid drugs?
Agranulocytosis
33
Indications for radioactive iodine to tx Graves
Larger thyroid gland
High TSI titers
Multitude of symptoms
High thyroxine lvls
34
Multinodular goiter
Most common in elderly, areas of iodine insufficiency
35
Common mutation of multinodular goiter
Somatic mutation in thyrotropin or TSH receptor
36
Multinodular goiter atypical presentation (elderly)
Weight loss, loss of appetite
Constipation
Cardiac symptoms (often presentation)
Tremor
37
Pemberton sign
Obstruction causes a superior vena cava syndrome
| Associated with multinodular goiter
38
Multinodular goiter labs
Suppressed TSH
| Elevated or normal T4
39
What imaging is important with obstructive symptoms in multinodular goiter?
CT
40
Multinodular goiter Tx
Radioactive iodine - TOC, CI in preggers
Anti-thyroid meds
Surgery
41
Mainstay imaging of a solitary thyroid nodule
Radionuclide
Cold - hypofunctioning
Warm - normal
Hot - hyperfunctioning
42
Dx tool of choice for evaluating thyroid nodule
Fine needle aspiration biopsy
Accuracy closely related to carcinoma type
Poor with follicular
43
Features of papillary thyroid cancer
Most common
| Psammoma bodies
44
Features of medullary thyroid carcinoma
Derived from neural crest derived C cells
| Associated with MEN 2A and MEN 2B
45
Features of anaplastic thyroid cancer
Most aggressive
| Hurthle cells
46
Euthyroid sick syndrome
```
Acute, severe illness causing abnormal thyroid fn tests
T3/T4 usually low
TSH usually normal
rT3 elevated
TFT normal after illness resolves
```
47
TOC in hyperthyroid of preggers
PTU
48
Classic S/S of Diabeetus
```
Polyuria
Polyphagia
Polydipsia
Fatigue
Weight loss
```
49
S/S more common in Type I diabetes
```
Lethargy, stupor
Smell of acetone
Weight loss
Kussmaul breathing
N/V, abd pain
```
50
Diabetes dx criteria
Fasting blood glucose > or equal 126 mg/dL on 2 occasions
OR
Symptoms + random blood sugar of > or equal 200 mg/dL
OR
HbA1C or > or equal 6.5%
OR
2 hour oral glucose tolerance test of > or equal 200 mg/dL
51
Normal FBG and IGT values
Normal FGB < 100 mg/dL
| Normal IGT < 140 mg/dL
52
Pathophys of DM1
Insulin is functionally absent b/c of destruction of pancreatic beta cells due to lymphocytic infiltration (autoimmune)
Circulating antibodies to Langerhans cells
Can have anti insulin antibodies as well
HLA DR3 or HLA DR4
53
DM1 Labs
Circulating insulin low or absent
| Plasma glucagon very high
54
DM1 Tx
Insulin
Short acting - regular, lispro, aspart
Intermediate - NPH, lente
Long acting - glargine, detemir
55
What is the honeymoon phase of DM1?
Temporarily regain own insulin secretory capacity after initiation of insulin therapy or after treated DKA
Decreased exogenous insulin requirement
Lasts weeks to months but never permanent (like many marriages)
56
What is Dawn Phenomenon?
Hormones (Cortisol, GH, Cates) released in early morning hours cause liver to release glucose
Lack of circulating insulin = high blood glucose
57
What is Somogyi Effect?
Night time hypoglycemia causes nocturnal glucose release by liver
58
How do you differentiate between Dawn and Somogyi?
Check BG at 2-3AM
Normal or high = Dawn
Low = Somogyi
59
Pathophys of DM2
```
Insulin resistance (hallmark of disease)
Related to elevated lvls of free FAs in blood that leads to decreased Glu transport into mm., increased hepatic Glu production, breakdown of fat
```
60
Possible findings in DM2
Acanthosis nigricans
Foot ulcers
Claw toes
61
What pts should be screened for DM2?
High risk pts:
High risk ethnic groups, women with large birth weight infant, pts with first degree relative, obese, high TGs and low HDL, polycystic ovary syndrome
62
DM2 Tx
Lifestyle modification
Meds
Insulin
Need to tx complications as well
63
Sulfonylureas
Insulin secretagogues
Greatest efficacy
AE: hypoglycemia
Glyburide, glipizide, glimeperide
64
Meglitinides
Short acting insulin secretagogues
Taken pre-prandial
Less hypoglycemia than biguanides
Repaglinide, Nateglinide
65
Biguanides
```
Reduce hepatic Glu production
Slight increase in insulin sensitivity
Associated with weight loss
Macrovascular improvement
Risk for lactic acidosis
Metformin
```
66
Metformin
Most common AE - diarrhea
Withhold in conditions predisposing to renal failure/hypoxia
CI in renal dysfn, liver dysfn, binge drinkers, hx of chronic metabolic acidosis
67
Alpha glucosidase inhibitor
Slow absorption of carbs
AE: flatulance
Acarbose, miglitol
68
Thiazolidinediones
```
Insulin sensitizers
Decrease TGs
Increase HDL, LDL
AE: Edema
Ros = possible increased risk of MI
Rosiglitazone, Pioglitazone
```
69
Incretin Mimetic
GLP-1 analogues
May use in combo with metformin, sulfonylureas
AE: GI
Exenatide, Liraglutide
70
Dipeptyl-peptidase IV inhibitors
DDP-4 degrades GLP-1
Monotherapy or in combo with met or thia
Sitagliptan, Saxipliptan
71
Goals of DM tx
FBS 80-120
HS 100-140
HbA1C < 7%
72
Microvascular complications of DM
Retinopathy
Neuropathy
Nephropathy
73
Macrovascular complication of DM
CAD
PVD
CVA
74
Common autonomic neuropathy symptom in DM
Orthostasis
| Tx: Midodrine
75
Tx for peripheral neuropathy in DM
Amitryptiline
Gabapentin
Pregabalin
Duloxitine
Check feet every vist
76
Tx for DM gastroparesis
Erythromycin
| Metocloperamide
77
Rate of decline in GFR in overt neuropathy for DM1 and DM2
Type 1 = 9.6 - 12
| Type 2 = 5.4 - 7.2
78
Tx of DM nephropathy
```
Glycemic control
HTN control (ACE, ARB)
```
79
Goals of Tx in CAD and Diabetes
```
Maximize glycemic control
Total cholesterol < 200
Total LDL < 100
Total HDL > 60
Total TG < 150
BP < 120/80
```
80
Who should be screened for gestational DM?
```
Women at high risk:
Severe obesity
Prior hx of GDM
Prior large for gestation age infant
Presence of glycosuria
Dx of PCOS
FHx of DM
```
81
When is the 100g OGTT positive?
Fasting > or equal 95 mg/dL
1 hr post prandial > or equal 180 mg/dL
2 hr post prandial > or equal 155 mg/dL
3 hr post prandial > or equal 140 mg/dL
82
Tx of GDM
Dietary therapy - multiple small meals, healthy snacks
Insulin therapy - regular, lispro, NPH, aspart
Oral agents - sulfonylureas, metformin
83
MODY
Autosomal Dominant
Mutations in genes encoding islet cell transcription factors for glucokinase
Age 10-25
84
Diabetes Ketoacidosis
Life threatening complication of diabetes
Type 1 >>>>>>>> Type 2
Severe dehydration in face of elevated blood sugars
Blood sugar > 250
pH < 7.3
Serum bicarb < 18 mEq/L
Ketonemia/ketonuria
85
Main fuel source of DKA
Ketones
| Body breaks down FAs since no insulin to break down high blood Glu
86
Symptom of acetone
Fruity breath
87
What exacerbates N/V in DKA?
Beta-hydroxy butyrate
88
Respiratory compensation in DKA?
Kussmaul respirations
89
Causes of mortality in DKA
Cerebral edema
MI
Electrolyte abnormality
ARDS
90
S/S of DKA
```
Dehydration
Fruity odor to breath
Kussmaul breathing
Change in consciousness
Signs of infection
```
91
Causes of DKA
```
Compliance
Infection - Klebsiella pneumonia
Surgical stress
Malfunction of pump
Idiopathic
```
92
DKA workup
Urine - ketones and C&S
Bloodwork
CXR
EKG
93
DKA Tx
FLUID
Initial replacement with isotonic saline
Switch to D5 0.45% NS as blood sugars approach 200 mg/dL
Insulin IV bolus followed by infusion - do not correct more than 100 mg/dL/hr
Electrolyte replacement -
K+ > 6 do not replace
K+ 4.5 - 6, replace 10 meq/hr
K+ 3 - 4.5 replace 20 meq/hr
K+ < 3 need to replace BEFORE starting insulin infusion
Only give bicarb if pH < 6.9
Tx underlying infection
94
Complications of DKA
Cerebral edema
Arrhythmia
Pulmonary edema
95
Hyperosmolar Nonketotic State
```
Impaired mental status
BG > 600 mg/dL
Profound dehydration
pH > 7.3
Serum bicarb > 15
Plasma osmolarity > 320 mOsm/kg
Ketones minimal
```
96
HNS
Type 2 >>>>>>>>>> Type 1
Often preceded by illness
Worsened/hastened by certain meds
Ex: Nursing home pt is ill, insulin or diabetic meds held but still getting diuretic
97
HNS complications
Cerebral edema
ARDS
Vascular complications
98
HNS Causes
MI or CVA
Infection
Diuretics
Dehydration
99
HNS Tx
```
Fluid replacement
Insulin infusion to SLOWLY correct hyperglycemia
Tx underlying dz/infection
Cardio-pulm monitoring
Neuro monitoring
```
100
Whipple's Triad
Documented low blood sugar
S/S of hypoglycemia
Reversal of symptoms with glucose
101
Factitious Hypoglycemia
Elevated insulin level
| Low C-peptide
102
Tx of hypoglycemia
Oral glucose, IM glucagon, IV glucose
| Surgery if insulinoma
