Endocrine 1-3 Flashcards
1
Q
What is the normal range for a fasting glucose?
A
70-100 mg/dL
2
Q
When can T1D be diagnosed up to?
A
Age 30
3
Q
Who has a higher risk of T1D?
A
Scandanavians
4
Q
What is the risk of T1D if its the offspring of an affected mother?
A
1-4%
5
Q
What is the risk of T1D if its the offspring of an affected father?
A
3-8%
6
Q
What is the risk of T1D if its a non-twin sibling?
A
3-6%
7
Q
What is the risk of T1D if its a monozygotic twin?
A
30%
8
Q
What is the risk of T1D if its a dizygotic twin?
A
8%
9
Q
What are some environmental factors that can increase your chance of getting T1D?
A
Viral infections (enterovirus), immunizations, cow’s milk early, high SES, obesity, Vit D deficiency
10
Q
What are some perinatal factors that can increase your chance of getting T1D?
A
Maternal age, preeclampsia, neonatal jaundice
11
Q
What genetic region is involved in risk factors of T1D?
A
HLA region of genome (Human Leukocyte Antigen)
12
Q
What happens when genetic and environmental factors trigger T1D?
A
T cells are activated, causes a proinflammatory response. End up with B cells producing autoantibodies
13
Q
What are the classic signs and symptoms of T1D?
A
Polyuria, polydipsia, weight loss, fatigueq
14
Q
What is the normal function of insulin?
A
Causes the entry of glucose into tissues, promotes storage of carbohydrates and fat
15
Q
What does insulin inhibit?
A
Lipolysis, glycogenolysis, and tissues catabolism
16
Q
What is the normal function of glucagon?
A
Stimulates glycogenolysis and gluconeogenesis
17
Q
Glucagon stimulates the breakdown of what?
A
Glycogen, used when blood sugar is LOW
18
Q
What is the pathophysiology behind T1D?
A
Abnormal glucose homeostasis. There is a relative or absolute reduction in insulin secondary to beta cell dysfunction
19
Q
What are the two factors causing beta cell dysfunction
A
Immune mediated (T cell) and idiopathic
20
Q
What does polyuria cause?
A
Increased urinary glucose excretion -> osmotic diuresis and hypovolemia
21
Q
What is the renal threshold for urine in the blood?
A
180
22
Q
What happens after the renal threshold for glucose is reached?
A
If blood sugar is higher than 180, the kidneys dump the glucose into the urine. Once it goes to urine, water follows, causing excessive peeing
23
Q
What does polydipsia cause?
A
Increased serum osmolality and hypovolemia
24
Q
Why does a patient with polydipsia become hypovolemic?
A
Water is leaving the blood volume, patient gets dehydrated. The serum osmolality is increased because there is less water
25
What does weight loss in T1D cause?
Hypovolemia and increased catabolism
26
How does catabolism cause damage?
Causes weight loss, if there are no carbs to use, the body begins to break down fat and protein
27
What is another classic sign of T1D?
Fatigue- there is no sugar left in the cells b/c its all in the blood, no energy!
28
What si/sx would be noted in an initial diagnosis of T1D?
Polyuria, polydipsia, weight loss, fatigue, weakness, blurry vision, frequent infections
29
Why would someone with T1D have blurred vision?
Hyperglycemia causes the eye lens to swell and can distort the vision
30
Why would someone with T1D have frequent infections?
Dysregulated immune system, and bacteria love sugar
31
What physical exam findings would be noted in an initial diagnosis of T1D?
Low BP, hypovolemia, tachycardia, could have a high respiratory rate due to acidosis, ketones on breath, abdominal pain is common
32
What tools do you need to make a diagnosis of T1D?
Check capillary blood (need one of the following):
Random blood glucose >200 with associated symptoms
Fasting blood glucose > 126
>200 on glucose tolerance test
33
What is the leading cause of morbidity and mortality in children with T1D?
Diabetic Ketoacidosis (DKA)
34
What are the causes of DKA?
Hyperglycemia (BS>200), metabolic acidosis (pH <7.3 OR bicarb <15), ketosis
35
What is ketosis?
Ketones spilling into the urine. If in urine, it will also be in the blood
36
What are some si/sx of DKA?
Vomiting, Tachypnea, Abdominal pain, SOB, Mental status changes (change in LOC)
37
What can someone with DKA appear to have?
Influenza!
38
Why does someone with DKA have abdominal pain?
Metabolid decomposition
39
What will the vitals look like for someone with DKA?
Low BP, weak diminished peripheral pulses, elevated pulses
40
What labs should be ordered for someone with DKA?
Blood glucose (>200), Ketones, Electrolytes (Na and K), Lactate, BUN, Creatinine, Venous pH, CBC
41
Why should a lactate be ordered on someone with DKA?
Lactate is released during tissue catabolism
42
Why should a BUN or Creatinine be ordered on someone with DKA?
Kidney function tests to see if in kidney failure, dehydration puts them at risk
43
What is the venous pH test for in DKA?
For the acidosis diagnosis
44
What 4 things need to be managed when someone has DKA?
1. Dehydration
2. Hyperglycemia
3. Sodium
4. Potassium
45
How do you manage dehydration when someone is in DKA?
Osmotic diuresis (glucose and ketones in urine) need CAUTIOUS fluids:
Gradual rehydration with isotonic fluid
Recommendation: 10mL/kg over 1 hour (max 1000mL)
46
How do you manage hyperglycemia when someone is in DKA?
Insulin infusion of 0.1units/kg/hour
| Once <300 change fluids to contain glucose (5% dextrose nl saline)
47
How do you manage sodium when someone has DKA?
Needs to be monitored, as H20 moves into cell, serum Na will rise
48
How do you manage high potassium when someone has DKA?
Give insulin, will go down to normal
49
How do you manage normal potassium levels when someone has DKA?
Give K with insulin, if you give just insulin then the potassium levels will drop
50
How do you manage low potassium when someone has DKA?
Give potassium first, then insulin. If insulin first: they will go into cardiac arrest
51
What does insulin do to potassium?
Insulin drives potassium into the cell, if its low and you give insulin, it will continue to drive it into the cells and cause very low levels. Risk of cardiac issues with low K
52
What other bloodwork can be considered once the T1D diagnosis has been made?
T1D antibodies: anti-pancreatic antibodies like insulin, GAD, IA2
Thyroid antibodies
Celiac: Anti-endomysial antibodies, tissues transglutaminase antibodies
53
What are the T1D antibodies?
GAD: glutamate decarboxylase, enzyme produced by beta cells
IA2: insulinoma autoantibody, produced within beta cells
54
What medications are used for T1D?
Insulin** both basal and prandial to keep glucose levels down and glucagon for emergent cases of hypoglycemia
55
What type of insulin is basal?
Long acting
56
What type of insulin is bolus?
Short acting
57
What are the examples of Short acting insulins (bolus) (4)
1. Aspart
2. Glulisine
3. Lispro
4. Regular
58
What are the examples of Long acting insulins (basal) (3)
1. Detemir
2. Glargine
3. NPH
59
What other lifestyle changes will patients with T1D have to make?
Frequent blood sugar checks 6-8x/day, nutrition counseling, exercise, need to know when to check ketones (BS>300, sick)
60
What type of nutrition changes will patients on T1D have to make?
CARB counseling: calculating insulin needs based on amount of carbs they are going to eat
61
What does it feel like to be hypoglycemic?
Shaky, teeth chattering, dizzy, tired, thirsty, irritable, going to bathroom frequently, HA, blurred vision zoned out
62
What is the most common cause for hypoglycemia?
Took their mealtime insulin and forgot to eat, exercise
63
What are the two physiologic causes of hyperglycemia?
1. Dawn phenomenon
| 2. Somogyi effect
64
What is the Dawn phenomenon?
When the blood sugars are high in the morning. its a surge of hormones daily around 4-5am (Cortisol) which increases blood glucose levels
65
How do you fix Dawn phenomenon?
Adjust the overnight basal insulin to decrease hyperglycemia in the morning
66
What is the Somogyi effect?
The patient goes low around 1-2am, hormones begin to surge (cortisol, catecholamines) in response to hypoglycemia, causing hyperglycemia in the morning
67
If the patients blood sugar is normal around 1-2am, which problem is it?
Dawn phenomenon
68
If the patients blood sugar is low around 1-2am, what is the problem?
Somogyi effect
69
How do you fix the Somogyi effect?
Have to pull back on the basal rate of insulin
70
What is carb counting?
45-60G of carbs at a meal, ratio of insulin for carbs is determined by th emedical provider
71
What are some examples of 15g of carbs?
4oz fresh fruit, 1 slice bread, 1/3 cup of pasta, 8oz milk
72
What is glycemic index?
Carbs with a low GI (0-54) good for T1D
73
Why are carbs with a low GI good for T1D?
Feel less hungry, provide you with more energy, lead to weight loss, provide a reduced risk of diabetes
74
What needs to be regularly checked for T1Ds?
Hypoglycemic events, annual eye checks, foot care, renal bloodwork (BUN, creatinine), lipids (CVD and cholesterol), A1c every 3 mos, dental (cavities), psyc (if needed)
75
What are some possible complications with T1D?
Diabetic retinopathy, peripheral neuropathy, nephropathy, skin complcations
76
What is non-proliferative diabetic retinopathy?
Dilation of small vessels, vascular closure leading to ischemia and increased permability
77
Which type of diabetic retinopathy is initial?
Non-proliferative
78
Which type of diabetic retinopathy has microaneurysms, hemorrhages, "cotton wool" spots, lipid exudates
Non-proliferative
79
Asymptomatic diabetic retinopathy
Non-proliferative
80
What happens in proliferative diabetic retinopathy?
Abnormal vascular proliferation (neovascularization)
81
Which type of diabetic retinopathy has a worse visual prognosis?
Proliferative
82
Neuropathy from T1D characteristics
Symmetrical sensory polyneuropathy, can begin in prediabetes state, effects the distal lower extremities
83
Where does the neuropathy in T1Ds start?
In the longest axons first, the sensory loss ascends. From the mid-calf it begins in the hands
84
What will be found on an exam with T1D neuropathy?
Vibratory sensation loss, altered proprioception, impaired pain, light touch, and temperature, decreased reflexes
85
What is the pathophys behind nephropathy in T1Ds?
Mesangial expansion, glomerular basement membrane thickening, podocyte injury, glomerular sclerosis
86
What are the si/sx of someone with T1D nephropathy?
Albuminuria, sometimes hematuria
87
T1D and nephropathy
Up to 30% will have increased albuminuria after 15 years duration of T1D, less than half of these will progress to nephropathy
88
What is macrosomia?
Increased glucose across the placenta, fetus makes more insulin so the baby is very large.
89
Insulin resistance, impaired insulin secretion, and increased glucose production are all part of what?
Type 2 Diabetes
90
What is typically a disease of adulthood but now also is seen more frequently in children and adolescents?
Type 2 Diabetes
91
What is T2D associated with?
Obesity
92
Circulating endogenous insulin is usually sufficient for what in T2D?
Sufficient to prevent ketoacidosis, but NOT sufficient enough to prevent hyperglycemia
93
What is the risk associated with T2D and monozygotic twins?
Over 40 years old, 70%
94
How many genetic loci have been associated with an increased risk of T2D?
30
95
What is the most important environmental factor causing insulin resistance?
Obesity
96
What are 3 potential sources of T2D?
1. Dysregulation or deficiency on release of insulin by beta cells
2. Inadequate or defective insulin receptors
3. Production of inactive insulin or insulin that is destroyed before it can carry out its function
97
What causes the starvation of body cells, breakdown of fat and increased protein?
The inability to transport glucose into fat and muscle cells (T2D)
98
T2D is the leading cause of what?
ESRD, non-traumatic lower extremity amputations, adult blindness
99
What screening tests are used to diagnose T2D?
FPG >126, random blood glucose >200, A1c >6.5%, two hour plasma glucose >200 during an oral glucose tolerance test
100
What are the test results for someone with prediabetes (T2)?
FPG 100-125, plasma glucose levels 140-199, A1c of 5.7-6.4%
101
What are prediabetes patients at risk for? (T2)
Increased risk of progression to T2D (6% per year), increased risk of CVD
102
How does the oral glucose tolerance test work?
Eat balanced diet (atleast 150g carbs) 3 days prior to test, drink 75-100g glucose, measured every hour after
103
What are normal glucose test results?
Normal BG at 1 hour is <184
| Normal BG at 2 hours is <140
104
What would the result from GTT be if patient was prediabetic?
If BG is 140-199 after 2 hours
105
What would the result from GTT be if patient was diabetic?
If BG was >200
106
What are some risk factors for T2D?
Family hx, BMI>25, physical inactivity, native/african americans, hx of gestational diabetes or baby >9lbs, PCOS, HbA1C 5.7-6.4%
107
Who should be screened for T2D?
All individuals >45 years old, if normal every 3 yrs after, earlier in certain individuals
108
People <30years old should be tested for diabetes if
BMI>25 or central obesity, habitually sedentary, 1st degree relative with DM, high-risk ethnic population, delivered baby >9lbs, HTN, HDL <35 or triglycerides >250, hx prediabetes, hx CVD
109
Which ethnic groups are high risk for T2D?
African american, latino/hispanic american, native american, asian american, pacific islander
110
What are the clinical presentations of T2D?
Polyuria, polydipsia, polyphagia
111
What complications can present with T2D?
Neuropathic, CV, chronic skin infections
112
What are some physical exam findings for T2D?
Obesity (central), HTN, eye hemorrhages, exudates, neovascularization, acanthosis nigricans, candida infections, decreased sensation to light touch, temp sensation and proprioception, loss of deep tendon reflexes in ankles, dry feet, muscle atrophy, feet ulcers
113
What is acanthosis nigricans?
Dark discoloration of the skin, hyperkeratotic
114
Patients with acanthosis nigricans patients also have what?
Defect in insulin receptor gene, extreme insulin resistance
115
What are some treatment goals of T2D?
Education, nutrition counseling, weight loss, microvascular and macrovascular complications, glycemic control, CV risk factor modification, increasing insulin secretion and responsiveness
116
CVD risk management for T2D
Smoking cessation, aspirin, BP control, management of dyslipidemia, diet, exercise
117
Routine health maintenance of T2D
A1c every 3mos, urine microalbumin yearly (kidney disease), podiatry referral, ophthalmology referral, self-monitoring of glucose levels with glucometer (1-4x/day)
118
What 1% drop in A1c is associated with what?
Improved outcomes form microvascular complications
119
Who has higher A1c targets?
Elderly, patients with multiple comorbidities and limited life expectancy
120
What are some nonpharmacologic therapies for T2D?
Weight reduction: carb controlled diet, regular meals with increase in protein, periodic snacks. No concentrated sugars
Exercise, surgical therapy
121
What is the first line pharmacological therapy for T2D?
Metformin (Biguanide)
122
Which two pharmacologic therapies lower glucose levels and improve insulin action?
Metformin and Thiazolidinediones
123
What two pharmacologic therapies stimulate insulin secretion from pancreatic beta cells?
Sulfonylurea and Meglitinides
124
What is an alternative first line therapy for T2D that can also be added to Metformin?
Sulfonylurea
125
Which pharmacologic therapy slows the intestinal absorption of glucose?
Alpha-glucosidase inhibitors (Acarbose, Miglitol)
126
Which pharmacologic therapy mimics the incretin effect or prolongs incretin action?
Glucagon-like peptide 1 (GLP1) therapies
127
What is the MOA of Metformin?
Reduces hepatic gluconeogenesis and improves insulin sensitivity
128
What is a C/I for Metformin?
Avoid in pts with renal insufficiency (CrCl <30ml/min)
129
Side effects of Metformin
Low risk of hypoglycemia, lactic acidosis (rare)
130
How does Metformin cause lactic acidosis?
Impairs lactate uptake by liver (avoid in liver failure)
| In renal failure patients, reduction in metformin excretion, lactate excretion
131
What is the mechanism of Sulfonylureas?
Stimulates insulin release, reduces serum glucagon, increases insulin binding
132
What are the 3 Sulfonylureas?
Glyburide, Glipizide, Glimepiride
133
What are some relative contraindications for sulfonylureas?
Hepatic or renal insufficiency (increase risk of hypoglycemia)
134
Side effects of sulfonylureas
Weight gain, hypoglycemia
135
What is the mechanism for Meglitinides?
Increase insulin secretion at beta cells
136
What are the 2 meglitinides?
1. Repaglinide (Prandin)
| 2. Nateglinide (Starlix)
137
Where is Repaglinide (Prandin) metabolized?
Hepatically and 90% excreted in the feces
138
Where is Nateglinide (starlix) metabolized?
Hepatically with renal excretion of active metabolites
139
Side effects of meglitinides?
Hypoglycemia, less likely than with sulfonylureas
140
C/Is of meglitinides
Nateglinide: renal dysfunction
141
What can meglitinides be added onto?
Metformin for patients with allergy to sulfonylurea
142
What is an example of an alpha-glucosidase inhibitor?
Acarbose and Miglitol
143
Side effects and C/Is of alpha-glucosidase inhibitors
Flatulence, diarrhea
| Careful in kidney insufficiency
144
Mechanism of Thiazolidinediones?
Sensitize peripheral tissues to insulin
145
Examples of thiazolidinediones?
Rosiglitazone (avandia) and Pioglitazone (actos)
146
Side effects of Pioglitazone
HF/edema, osteoporosis/fractures, possibly bladder cancer, weight gain
147
Mechanism of GLP-1 agonists
Enhance glucose dependent insulin secretion, slow gastric emptying, reduce postprandial glucagon
148
Examples of GLP-1 receptor agonists
Exenatide (byetta) and Liraglutide (Victoza)
149
What is the BBW for GLP-1 receptor agonists?
Causes medullary thyroid cancer in mice
150
GLP-1 receptor agonists
Supresses glucagon secretion, administered by subq injection, low risk of hypoglycemia, $$$
151
What are examples of DPP-4 inhibitors?
Sitagliptin (januvia)
Saxagliptin (Onglyza) possibly causes HF
Linagliptin (tradjenta)
Alogliptin (nesina)
152
Are DPP4- inhibitors first line treatment?
No, can be monotherapy in pts who cant take Metformin, SUs, or thiazolidinediones
153
When should a second agent be added to someone with T2D?
If/when A1c goal <7% is not achieved within 3 mos of initial therapy
154
When should you switch to insulin? T2D
When A1c is >8.5
155
What is HHNK?
Hyperglycemic Hyperosmolar State (Hyperosmotic Hyperglycemic Non-ketonic State)
156
HHNK results in what?
Hypovolemia and electrolyte abnormalities
157
What can cause HHNK?
Major illnesses: MI, CVA, sepsis, pancreatitis
Drugs: Glucocorticoids, thiazides, atypical antipsycs
Compliance issues
158
What is the clinical presentation of HHS? (Hyperglycemic Hyperosmolar State)
Polyuria, polydipsia, weight loss, lethargy, decreased skin turgor, dry mucous membranes, tachycardia, hypotension
159
What are some abnormal lab results of HHS?
>1000 BS, hyperosmolarity, pre-renal azotemia (volume depletion), low potassium, magnesium and phosphate
160
What lab values are different in HHS (T2D) than in DKA (T1D)?
Acidosis and ketonemia are absent or mild in HHS
161
What is the treatment for HHS?
Intravenous insulin infusion, IV fluid, electrolyte monitoring and repletion (K, Mg, phosphate)
162
Long term microvascular complications of T2D are what
Retinopathy (leading cause of blindness in US), Nephropathy (can progress to ESRD required dialysis), Neuropathy (pain and numbness of lower extremities) and Gastroparesis (ulcers can lead to amp)
163
What are the long term macrovascular complications of T2D?
Peripheral vascular disease, lower extremity ulcers, amputations (infected ulcers), CAD, MIs
164
How do you treat the Dawn phenomenon with T1D?
Increase the basal insulin
165
How do you treat the somogyi effect with T1D?
Decrease the overnight basal insulin
166
What is the adrenal gland separated into?
Superficial adrenal cortex and inner adrenal medulla
167
The adrenal cortex is a true what?
Endocrine gland
168
The adrenal medulla is a modified what?
Sympathetic ganglion
169
What part of the spinal cord innervates the adrenal medulla?
T5-T11
170
What are the 3 main types of hormones produced by the adrenal cortex?
Glucocorticoids, Mineralocorticoids, Androgens
171
The Zona Fasciculata produces what?
Glucocorticoids
172
The Zona Glomerulosa produces what?
Mineralocorticoids
173
The Zona Reticularis produces what?
Androgens
174
Why type of corticosteroid is involved with DHEA and androstenedione?
Androgens (precursors to testosterone)
175
What role does aldosterone play?
Causes sodium retention into serum with water and potassium secretion into the renal tubule
176
What does aldosterone maintain?
Blood pressure
177
Which corticosteroid is involved with aldosterone?
Mineralocorticoids
178
What is gluconeogenesis?
An increase in glucose metabolism and glycogen formation, especially in the liver
179
What do glucocorticoids do?
Mobilize fat, protein and carbs. Suppress the immune system through anti-inflammatory pathways
180
When is cortisol released?
Released at a basal rate with bursts due to a stress response
181
What is cortisol regulated by?
Anterior pituitary and ACTH via negative feedback loop
182
Corticosteroids are all synthesized from what?
Cholesterol
183
What factors can reduce cortisol levels?
Music/massage therapy, omega-3 fatty acids, mg supplementation with aerobic exercise, dancing regularly, high dose VitC
184
What factors can increase cortisol levels?
Caffeine, sleep deprivation, intense or prolonged aerobic exercise, trauma/stressful event, subQ adipose, anorexia nervosa, excessive alcohol intake
185
What catecholamines are released by the adrenal medulla?
Epinephrine, norepinephrine, dopamine
186
What are chromaffin cells?
In the adrenal medulla, they are the modified post-ganglionic neurons that have a direct connection to the sympathetic division of the ANS
187
What is effected with the "fight" response
Increased BP, HR, vasoconstriction dermis/GI tract, vasodilation smooth muscle (bronchioles, capillaries), glucose metabolism
188
Why are the medullary/chromaffin cells clustered around large vessels?
Cause a direct rapid release of catecholamines that target receptors throughout the body
189
Why is there increased muscle contractility in the fight or flight response?
To provide the body with extra speed and strength and faster reflexes
190
Pheochromocytoma is a tumor found where?
Rare adrenal medulla tumor
191
What does the pheochromocytoma tumor produce?
Produces, stores and secretes catecholamines
192
5% of pheochromocytomas are associated with what?
MEN2a and MEN2b
193
What is a common clinical feature of pheochromocytoma?
HTN: sustained (60%) or labile
| Other sxs: HA, diaphoresis, palpitations
194
What are some other non-common si/sx with pheochromocytoma?
Chest pain, N/V, abdominal pain, apprehension.anxiety with feeling of impending doom, pallor and/or flushing, HTN +/= tachycardia
195
What can be used to diagnose pheochromocytoma?
```
24 hour urine collection metanephrine, VMA, total catecholamines, creatinine (levels should normally be low)
Abdominal CT scan (85-95% sensitivity)
Abdominal MRI (99% sensitivity)
```
196
What drugs need to be given for pheochromocytoma before surgery and why?
Alpha-adrenergic blockade 10-14 days and Beta-adrenergic blockade 2 days prior to prevent intra-operative HTN crisis
197
What alpha blocker can be given for pheochromocytoma patients pre-op?
Phenoxybenzamine HCl (Dibenzyline)
198
Which beta blockers can be given for pheochromocytoma patients pre-op?
Propranolol or Nadolol
199
Laparoscopic surgery is preferred for pheochromocytoma tumors unless what?
Unless >8cm
200
What syndrome is the hypersecretion of aldosterone?
Hyperaldosteronism
201
Primary Hyperaldosteronism involves what?
Due to a problem with the adrenal glands. Could be due to hyperplasia or an adenoma
202
What level is the plasma renin at in primary Hyperaldosteronism?
Low. BP goes up, there is increased flow through the JGA and kidney, causes the renin to DROP
203
Secondary Hyperaldosteronism involves what?
Extra-adrenal etiology, plasma renin HIGH
204
Pathophys behind secondary Hyperaldosteronism
Appropriate release of aldosterone, patient has low flow through JGA causing HIGH renin and aldosterone
205
What can cause secondary Hyperaldosteronism
Liver failure patients with ascites, nephrotic syndrome, chronic low flow
206
What does angiotensin 2 do?
Increases sympathetic activity, causes tubular Na and Cl reabsorption, K excretion and water retention, causes aldosterone secretion from adrenal gland, arteriolar vasoconstriction, increase BP, ADH secretion from pituitary gland and water absorption in collecting duct
207
What is the mechanism of an ACE I
Angiotensin converting enzyme inhibitors,
208
What is the mechanism for ARBs
Angiotensin receptor blocker (angiotensin 2 on receptor)
209
What is Conn's syndrome?
Primary Hyperaldosteronism, adrenal adenoma with bilateral cortical nodular hyperplasia
210
What are the 4 classic findings of Conn's syndrome?
1. Diastolic HTN (HAs)
2. Hypokalemia (muscle weakness and fatigue)
3. Metabolic alkalosis (Excess H+ secretion = HCO3 elevation)
4. Low plasma renin
211
What does the hypersecretion of aldosterone cause?
Increased renal tubular exchange of sodium and H+ secretion
212
What will bloodwork show if someone has primary Hyperaldosteronism?
Hypokalemia, hypernatremia, metabolic alkalosis (loss of H+ in urine and shift H+ into cells), low plasma renin
urine: proteinuria
213
What will an EKG show for primary Hyperaldosteronism?
U waves, ectopic beats, ST depression, prominent P wave, prolonged PRI, LVH criteria
214
What will a CXR show for primary Hyperaldosteronism?
Cardiomegaly
215
What does increased aldosterone do (primary Hyperaldosteronism)
Increased aldosterone causes increased sodium retention, increases the volume, drops the renin levels
216
What are some diagnostic tests used for primary Hyperaldosteronism
Renin hyposecretion w/volume depletion, failed aldosterone suppression w/volume expansion, Abd/pelvic CT or MRI
217
Therapy for primary Hyperaldosteronism
Adenoma: surgical excision
| Diet with sodium restriction and aldosterone antagonist (Spironolactone)
218
What is the criteria for diagnosis of primary Hyperaldosteronism?
Diastolic HTN without edema, decreased secretion of renin when stimulated, increased secretion of aldosterone that cannot suppress, no diuretic use
219
What are some causes for secondary Hyperaldosteronism?
Edema state like nephrotic syndrome, ascites, CHF (severe)
| Associated with HTN: renin overproduction
220
What can be a cause of low flow through the JGA?
Renal artery stenosis
221
Pathophys of secondary Hyperaldosteronism
Decreased volume causes an increase in renin, causing an increased in aldosterone which leads to sodium retention
222
What is the cause of Cushing's syndrome?
Prolonged exposure to endogenous or exogenous glucocorticoids
223
Hypersecretion of cortisol from the adrenal cortex causes what?
Pituitary overproduction of cortisol from the adrenal cortex (Cushing's Disease)
224
Pituitary overproducing cortisol is caused by what?
Pituitary tumor
225
What else can a pituitary tumor cause?
Bitemporal hemianopsia/optic chiasm compression. Also can cause decreased TSH, FSH, LH, GH, prolactin
226
What are some other endogenous causes of cushings syndrome?
Adrenal primary mass (typically adenoma and ACTH independent), SCLCA small cell lung carcinoma producing ACTH, thyroid neoplasm, pancreatic neoplasm
227
Hx of cushings disease would have what in it?
Weight gain (buffalo hump), dermis changes, proximal muscle wekaness/wasting, sexual dysfunction, psychiatric manifestation, tumor symptoms, increase infections, poor wound healing, osteoperosis and pathologic fractures
228
What type of sexual dysfunction can happen with Cushings syndrome?
Decreased libido, impotence, irregular menstruation, infertility, OR virilization female, feminization male (adrenal mass suggested)
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What dermis changes can happen with Cushings syndrome?
Purple/red striae, think skin, easy bruising
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What tumor symptoms can be seen with Cushings syndrome?
HA, vision changes, polyuria, cognitive dysfunction
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What can be seen on PE with Cushings syndrome?
Adipose deposition/obesity, dermis changes, CV/renal HTN edema, PUD, galactorrhea, hypothyroid sxs, fractures/proximal muscle weakness, psyc manifestations
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Diagnostic tools for Cushings disease
24 hour urine cortisol, 1mg Dexamethasone suppression test, CRH/Dex suppression test if above are inclusive, ACTH level
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What would a 24hour urine cortisol show if pt had Cushings Dx?
>300mcg/dL
| <90 is normal
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What is the 1mg Dexamethasone-suppression test?
Dexamethasone is given at 11pm and the cortisol is then measured at 8am
Cushings will show high cortisol and ACTH
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What is the CRH/Dex suppression test and what will it show if the patient has Cushings?
If the cortisol is >50, diagnostic for Cushings
236
What should the ACTH level be at normally around 4pm?
Low
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What should you do if the ACTH level is high?
Cranial MRI and high dose dex-suppression test
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What should you do if the ACTH level is normal?
Abdominal CT/MRI
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What are the two ways to treat Cushings
Surgical resection and medical management
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What is the goal of surgical resection in Cushings disease?
Culprit tumor is reseted. Typically transphenoidal resection of pituitary mass
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What can you do if the surgical resection for Cushings Dx does not work?
Consider radiation of pituitary
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What types of meds can be used for Cushings Disease?
Ketoconazole: Decreaes cortisol production @p450 enzymes of liver
Metyrapone: Blocks final step of cortisol synthesis
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What are the SEs of using ketoconazole for Cushings?
HA, sedation, N, decreased libido, impotence, gynecomastia, elevated LFTs, irregular menses
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Addisons disease is what type of insufficiency?
Adrenocortical due to destruction or dysfunction of the adrenal cortex
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What can cause Addisons disease?
Idiopathic autoimmunity (80%), TB, hematologic malignancy, AIDS, drugs (methadone, ketoconazole), abdominal radiation therapy, CAH (congenital adrenal hyperplasia)
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The two most common causes of Addisons disease?
Idiopathic autoimmunity and TB
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What can be seen in the clinical presentation of Addisons?
Slow insidious presentation: weakness/fatigue, hypotension orthostasis dehydration, weight loss/anorexia, +/- hyperpigmentation of skin and mucosa, N/V/D/abd pain
248
How can we diagnose Addisons disease?
Cortrosyn Stimulation Test (Cosyntropin)
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What is Cortrosyn stimulation test?
ACTH stimulation test-tests functional ability of adrenal cortex to synthesize cortisol
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How is the Cortrosyn stimulation test done?
Check baseline plasma cortisol and aldosterone levels
inject IV ACTH o.25mg
30min and 60min post-injection check plasma cortisol and aldosterone levels
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What will the results be from the cortrosyn stimulation test if the patient has Addisons?
There will be minimal to no change in the cortisol or aldosterone levels
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What will the electrolytes shows if someone has Addisons?
Hyponatremic, Hyperkalemic, increased urine Na, increased BUN/Creatinine
253
Other lab findings for Addisons Disease
Elevated TSH, should do CXR and PPD, CT abdomen could see enlarged calcified or atrophic adrenal glands
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What would the cause be if the abdominal CT showed enlarged adrenals?
TB, fungal infection, hemorrhage
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What would the cause be if the abdominal CT showed calcified adrenals?
TB, histoplasmosis
256
What would the cause be if the abdominal CT showed atrophic adrenals?
Idiopathic autoimmunity
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What is primary adrenal insufficiency?
Anatomic destruction or metabolic failure of the adrenal cortex
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What is secondary adrenal insufficiency?
Suppression or disease of hypothalamic-pituitary axis (ACTH deficiency)
259
What are the signs for secondary adrenal insufficiency compared to Addisons?
Similar symptoms but no hyperpigmentation
260
What can be some causes of secondary adrenal insufficiency?
Panyhypopituitarism, prolonged exogenous steroids
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How do we treat adrenal insufficiency?
Glucocorticoid: Hydrocortisone 20-30mg/day divided to stimulate diurnal adrenal rhythm 2/3 am and 1/3 pm
Mineralocorticoid: Fludrocortisone 0.05-0.1mg/day with ample sodium intake
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If there is a rapid/severe adrenal crisis, what can happen?
If untreated, coma and death
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What causes adrenal crisis typically?
Exacerbation of chronic adrenal insufficiency (stress precipitant or sudden withdrawal of chronic steroid)
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What else can cause adrenal crisis?
Acute hemorrhagic destruction of bilateral adrenal glands.
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What is Waterhouse-Friderichsen Sydrome?
Adrenal crisis that can be caused by pseudomonas, meningococcemia septicemia
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What are some stressors with adrenal crisis?
Infection, trauma, surgery, V/D, emotional turmoil
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Symptoms of adrenal crisis
Hypotension -> vascular collapse
| N/V/adb pain, hyperpyrexia, lethargy somnolence MS change, hypoglycemia, hyponatremia, hyperkalemia, metabolic acidosis
268
How do you treat adrenal crisis?
IVF resuscitation 2L NS followed by D51/2Ns
| Stress Hydrocortisone 100mg IV q6hours or Dexamethasone 4mg q24hours
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What are the 3 Ps for MEN type 1
Hyperparathyroid, Pancreatic islets, Pituitary
270
MEN
Multiple Endocrine Neoplasm
271
Hyperparathyroid in MEN type 1
Most common manifestation
Due to hyperplasia or adenoma
Sxs: Hyperglycemia, elevated serum Ca++ and PTH normal
272
Pancreatic islets in MEN type 1
Occurs in parallel with hyperparathyroid
Due to: hyperplasia, adenoma, or carcinoma
Increase production of pancreatic islet cell hormones like gastrin, insulin, glucagon, VIP
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Pituitary in MEN type 1
Prolactin-> Prolactinoma
GH -> ACromegaly
ACTH -> Cushings disease
274
How do you diagnose MEN type 1?
With hormone/electrolyte assays, provocative tesitng, and radiologic testing
275
Which hormone/electrolyte assays are used to diagnose MEN type 1?
Gastrin, glucagon, Ca++ and PTH levels, hypokalemia, hypochloremia, metabolic acidosis, GH, prolactin level, ACTH level
276
Which provocative tests can be used to diagnose MEN type 1?
Secretin stimulation test w/gastrin levels, short or 72hour fast w/serum insulin and c-peptide levels, dexamethasone suppression test
277
What radiologic tests can be used to diagnose MEN type 1?
CT/MRI
278
Which therapies can be used for MEN type 1?
Surgical resection and medical management
279
What type of surgical resection is used for MEN type 1
Transphenoidal approach w/ pituitary tumors (often difficult b/c multicentric)
Parathyroidectomy and thyroidectomy
280
What meds are used for MEN type 1?
```
Dopamine agonists (Bromocriptine/ Cabergoline) for prolactinoma
H2 receptor antagonist, PPI for ZES
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What is seen in MEN2?
Medullary thyroid carcinoma and pheochromocytoma
282
MEN2a usually involves what?
MTC, pheo (50%), hyperparathyroidism (15-20%)
| most common manifestation
283
When does MTC typically develop in 2a?
Childhood and >1cm tumor associated with local and distant metastasis
284
MEN2b involves what
MTC, pheo (50%), mucosal neuromas, marfanoid body habitus
285
When does MTC develop in type 2b?
Earlier and is more aggressive than 2a
286
MEN2 treatment
Early thyroidectomy, genetic testing, annual screening w/urine metanephrine/VMA, measurement with Ca++ PTH q 2-3years, surgery
287
What type of surgery is needed for treatment of MTC?
Total thyroidectomy w/central LN dissection
288
What type of surgery is needed for treatment of hyperparathyroidism?
Excise 3 1/2 with remnant in neck, full excision with remnant implanted in back of forearm
