Part 25 Flashcards
(170 cards)
1
Q
Wernicke’s aphasia
A
Classically localized to lesions affecting the posterior superior temporal gyrus, markedly impaired comprehension where speech is voluminous but meaningless often described as a word salad, usually speech retains normal cadence and intonation and patient apepars completely unaware of deficit
2
Q
Wernicke-Korsakoff syndrome
A
Associated with alcoholism, but can occur in other situations such as malnutrition or dialysis, classic triad is hoemorrhagic necrosis in midline brain structure producing deficits in mentaiton (encephalopathy), oculomotor function, and gait ataxia, administer thiamine as soon as expected as untreated results in death
3
Q
Anterograde amnesia
A
The impaired ability to formulate new memories
4
Q
Retrograde amnesia
A
Loss of all memories prior to an event
5
Q
Delirium
A
Acute change (hours to days) where a patient has fluctuating levels of consciousness easily confused with psychiatric disorders most often due to primary underlying causes such as a medical condition, medication or drug withdrawal
6
Q
Delirium diagnosis (4)
A
- NOT mini mental status exam
- confusion survey
- electrolytes, creatinine, tox screen, drug levels, etc (rule out)
- neuroimaging
7
Q
Most common medical etiologies of delirium (6)
A
- infection
- fluid and electrolyte disturbance
- withdrawal
- toxicity
- metabolic disturbances
- post op states
8
Q
Sundowning
A
Distinguished condition from delirium, frequently seen poorly understood phenomenon with frequent recurrence*** characterized by change in mental status and behavior often becoming more agitated as the day ends
9
Q
Dementia vs delirium
A
Insidious vs acute, stable and progressive vs fluctuating, sensorium intact till late vs impaired, poor short term memory vs globally impaired
10
Q
When I say amyloid plaques and neurofibrilary tangles you say…
A
….alzheimer’s disease
11
Q
Pick’s disease/frontotemporal dementia
A
dementia is initially manifested by changes in personality and social behavior or language progressing over time to a more global dementia, progresses more rapidly than alzheimer’s
12
Q
Dementia with lewy bodies
A
form of dementia is characterized by the presence of abnormal aggregates of protein that develop inside nerve cells. These are identified under the microscope when histology is performed on the brain, distinctive clinical features including visual hallucinations, parkinsonism, cognitive fluctuations, and dysautonomia, differentiated from parkinson disease because cognitive decline is manifested much earlier than motor symptoms
13
Q
Vascular dementia
A
Result of brain ischemia, no understood risk factors and not fully understood, no uniform diagnostic criteria, also referred to as post stroke dementia as clinical features are consistent with vascular etiology
14
Q
Parkinson disease dementia
A
Characterized by executive function (early findings include brady and akinesia, rigidity, etc) and sees memory loss as a later finding, most with parkinson disease will go on to develop this
15
Q
Sarcopenia
A
Decline in lean body mass often associated with age and a corresponding increase in total body fat that occurs in up to 50% of the elderly
16
Q
Leading causes of involuntary weight loss in the elderly (3)
A
- depression
- cancer
- benign GI disease such as dysphagia
17
Q
Cachexia
A
Inflammatory metabolic disorder with excess muscle loss and prostoglandin production throughout the body due to underlying condition, relatively rapid and giving characteristic emaciated appearance
18
Q
Oral/dental health problems that affect the elderly (3)
A
- dental caries
- periodontal disease
- xerostomia
19
Q
Vit A nutrition deficiencies side effects in elderly (3)
A
- dry skin
- bitots spots
- xeropthalmia
20
Q
Vit B6 nutrition deficiencies side effects in elderly (3)
A
- glossitis
- peripheral neuropathy
- anemia
21
Q
Elder abuse
A
Mistreatment for individuals generally greater than or equal to 60 years including abuse, neglect, or financial exploitation, perpetrated by those in an ONGOING relationship that involves expectation of responsibility toward a victim** (excludes abuse by strangers, has to be a caretaker of some form - doctor, taxi driver, family), can be physical (including neglect even self neglect), sexual, or psychological (majority)
22
Q
Decisional capacity
A
The ability to communicate a choice, understand relevant info, appreciate the situation and its consequences, and reason about treatment options
23
Q
Executive capacity
A
The ability to execute ones decisions
24
Q
Self neglect
A
Failure of vulnerable elder to provide for own care and protection (also called failure to thrive), excludes elderly who have capacity but choose not to
25
PE findings that indicate elder abuse (8)
- traumatic alopecia (hair pulled)
- SPIRAL FRACTURE in long bone***
- abrasions or skin tears
- burns
- lacerations
- evidence of restraint
- pressure ulcer
- pain or soreness in genital area or new onset STI
26
Mandatory elderly abuse reporting
-Ethical responsibility for provider to care for patients and document and report concern for elder misreatment, if suspected in a facility call the long term care ombudsman, if in the general population call adult protective services.
27
Secretion of insulin is triggered by these 5 things
- glucose
- amino acids
- fatty acids
- ketone bodies
- Epi/norepi
28
Absence of insulin transfers us from a ___ state to a ___ state
anabolic, catabolic (in absence of insulin we see glycogen converted to glucose, gluconeogenesis, and decreased cellular uptake of glucose)
29
Therapeutic uses of insulin (3)
- diabetes mellitus (type 1 all patients and some type 2)
- IV for diabetic ketoacidosis
- treatment of hyperkalemia (pulls K+ intracellularly
30
Recombinant human insulin analogs
Bioidentical insulin grown in e coli or yeast that has been slightly modified to have a different time course (either shorter or longer acting)
31
Rapid acting insulin analog time frame compared to regular
5-30 minutes, 30-60 (but have a shorter duration of action in 3-5 hours, are more convenient because can be administered with or just before a meal
32
Metformin (glucophage) function
-Drug of choice for initial treatment of type 2 diabetes, when not A1C goal reached can use additional agents depending on comorbidities (SGL2 inhibitors)
33
If max dose of 2 drugs insufficient to achieve glycemic control, then...
....insulin or another drug can be added
34
Principal differences between first and 2nd gen sulfonylureas
Second gen are much more potent at lower doses and serious interactions are less common and are therefore widely used and generally superior
35
3 second gen sulfonylureas
- Glipizide (glucotrol)
- glyburide
- glimepiride
36
Sulfonylureas mech of action
Stimulate release of insulin from pancreatic tissues by binding receptor sites on B cell causing depolarization triggering increase in intracelular calcium and thus insulin release (pancreas must be able to produce insulin for them to be effective, with prolonged use agents enhance cellular sensitivity to insulin thru unknown mechanism)
37
Sulfonylureas ADR's (4)
- Hypoglycemia (tell patients not to skip meals)
- weight gain 5-10 pounds
- hematologic reactions such as lekupenia or thrombocytopenia
- disulfuram like reaction (flushing, palpitations, nausea reported with use when drinking on chlorpropamide ( a gen 1 agent)
38
Metformin mech of action
- lowers blood glucose primarily thru decreasing hepatic gluconeogenesis and secretion of glucagon like peptide
- does not stimulate insulin release from pancreas and does not actively drive down blood glucose levels posing little to any added risk of hypoglycemia when used alone
39
Metformin therapeutic use (4)
- monotherapy in patients whose blood sugar levels are not controlled by diet or exercise alone
- combo therapy with other antidiabetic agents such as sulfonylureas
- PCOS off labeled use
- Cardiovascular reduction in risk of MI
40
Metformin ADR's (3)
- GI effects
- Decreased B12 and folic acid absorption which can lead to deficiencies (not recommended to supplement with metformin)
- Lactic acidosis in patients with low GFR
41
Acarbose (precose) drug class and mech of action
- alpha glucosidase inhibitor
- oral agent that reversibly inhibits alpha glucosidase, and enzyme present in brush border mucosa of small intestine, slows rate at which complex polysaccharides and sucrose are digested resulting in lower postprandial blood glucose conc
42
Acarbose (precose) ADR (1)
-GI effects due to fermentation of unabsorbed carbohydrate
43
Miglitol (glyset) function
Delays carb conversion of oligosaccharides and complex carbs to glucose decreasing postprandial rise in blood glucose
44
Thiazolidinediones function and mech of action
- Antidiabetic agents that work primarily by decreasing insulin resistance
- Decrease insulin resistance by activating a specific receptor type in the cell nucleus known as PPAR gamma, as a result insulin responsive genes are turned on that hep regulate carbohydrate and lipid metabolism, cellular response to insulin is increased promoting uptake
45
Thiazolidinediones ADR's (4)
- Uncertain if benefits outweigh risks
- Heart failure
- weight gain
- anemia
46
Rosiglitazone (avandia) drug class, function and ADR's (3)
- Thiazolidinediones
- Approved for monotherapy or with metformin for treatment of type 2 diabetes
- edema, weight gain, mild anemia
47
Pioglitazone (ACTOS) drug class, function, ADR's (3)
- Thiazolidinedions
- Approved for monotherapy or with metformin for treatment of diabetes
- Fractures, bladder cancer, hepatotoxicity
48
Metiglinides (Glinides) function
Short acting agents for type 2 diabetes with same mech of action as sulfonylureas, tend to be shorter acting tho and are taken with each meal
49
DPP-4 inhibitors mech of action and therapeutic use (1)
Promote glycemic control by enhancing the actions of incretin hormones, potentiating glucose dependent secretion of insulin and suppress glucagon secretion, produce modest reductions in A1C levels when used as monotherapy
-2nd line therapy as add on to metformin
50
Sitagliptin (Januvia) drug class, function, and ADR's (3)
- DDP inhibitor
- Approved for PO monotherapy or in combo with other antidiabetic drugs for treatment of type 2 diabetes
- URI, headaches, pancreatitis
51
SGLT2 inhibitors mech of action and other benefit
- Block SGLT2 transporters decreasing renal glucose reabsorption and increasing urinary glucose excretion, reducing fasting and prepreandial blood glucose levels
- Reduction in SBP reducing CV risk
52
SGLT2 inhibitors ADR's (3)
- frequent mycotic genital and urinary tract infection
- fournier gangrene (necrotizing infection of external genitalia, perineum, and perianal region)
- acute kidney injury
53
Glucagon like peptide 1 (GLP1) receptor agonists function and mech of action
- injectable agents administered SC for treatment of type 2 diabetes
- Have same physiologic effect as endogenous incretins slowing gastric emptying stimulation of glucose dependent release of insulin and inhibition of postprandial release of glucagon
54
GLP 1 agonist ADR's (2)
- pancreatitis
-medullary thyroid cancer
55
Pramlintide (symlin) drug class and function
- synthetic analog of human amylin (amylin mimetic)
- approved for adjunctive treatment for patients with type 1 or 2 diabetes who inject insulin at mealtimes and have failed to achieve glucose control
56
Lispro (humalog) rapid absorption mech of action
-unlike most insulin, avoids self association to form hexamers unlike most insulins and thus attains more rapid absorption and onset of action (15 min)
57
Regular insulin (humulin R) function
Unmodified crystalline insulin that is short acting soluble insulin, after SC injection forms small hexamers delaying absorption and onset to .5-1 hour, with peak action occurring 2.5-5 hours, and lasting 4-12 hours
58
Regular U-500 insulin function (Humulin)
Normal insulin indicated in patients who require >200 units/day specifically targeting insulin resistant patients with severe type 2 diabetes, exhibits both a bolus and basal effect and can be used as monotherapy in some cases for type 2 diabetics
59
Examples of long acting insulin (3)
- Lantus
- levemir
- toujeo
60
Lantus function
Long acting peakless insulin analog, mimics basal effects of insulin secreted by healthy pancreas
61
Administration of insulin
Must be given by injection or inhalation because it is degraded in the stomach as a peptide
62
Treatment of hypoglycemia in patients (3)
- oral sugar supplements (NOT chocolate or hard piece of candy - aspiration risk if loss of gag reflex or unconscious)
- IV dextrose
- Glucagon
63
2 causes of diabetic coma that must be determined
- hypoglycemic requiring withholding of insulin
- ketoacidosis which requires insulin
64
What is the leading cause of end stage renal disease?
Diabetic nephropathy
65
Characteristics of type 1 diabetes (6)
- Autoantibodies presence against B cells of pancreas
- Absolute insulin deficiency requiring supplementation
- Most common in youth
- acute onset
- Ketosis prone
- Genetic predisposition
66
Physiological serum insulin secretion profile
- Spikes after each meal before quickly lowering to low poinr (50% of insulin content)
- In the night time, see drop to low amount but never to zero because of glycogen breakdown and gluconeogenesis from the liver AND kidney** that occur during sleep causes need to keep some insulin up at all times (50% of insulin content)
67
Between meal and overnight (long acting) insulin options (peakless baseline, 1 shot a day) (5)
- levemir
- lantus
- tresiba
- toujeo
- basaglar
These are incredibly expensive, all made by bacteria and e coli from recombinant human insulin analog modified to be long acting
68
NPH insulin analog function
Given once every 12 hours (twice a day) to maintain closest to baseline, but does see a peak about 5-6 hours after administration, very cheap and affordable
69
Quick acting insulin analogue (normal insulin) function
-starts working in about half an hour (take about that amount of time before a meal), peaks within 2 hours, and then quickly drops off, concern if taken without a meal following shortly after
70
Immediate acting insulin analogues (3) and function
- aspart, glulisine, lispro
- Act almost immediately after taking, most closely mimics the body's insulin, so fast acting can be given after 10-15 min post meal and dosed corresponding to what percent of meal they ate (good to prevent giving before and then they don't eat and then we are screwed)
71
Typical starting dose for between meal and overnight insulin (long acting)
.3 u/kg
72
Advantages of continuous subcutaneous insulin infusion (4) and disadvantages (2)
- Programmable for meals and overnight
- greater flexibility of lifestyle
- fewer injections
- control as good as multiple daily injections if not better
- risk of ketosis from interruption
- complexity
73
Should a continuous subQ insulin infusion fail, patient needs to have what waiting at home?
-long acting insulin refrigerated (allows patient to get it in case of failure of pump, can then just inject pump manually to simulate for meals)
74
Sliding scale insulin regimens
-Chart that allows for blood glucose level to directly determine amount of insulin to be delivered to patient
75
Glycemic control in a hospital patient target range
144-180mg/dL
76
Diabetic ketoacidosis treatment options (4)
- restoration of volume
- correct acidosis (slower to correct than hyperglycemia)
- replenish K+
- correction of hyperglycemia
77
Risk factors for type 2 diabetes (1 big one and 6 others)
- first degree relative with DM***
- age >45
- obesity
- sedentary lifestyle
- hypertension
- dislipidemia
- Gestational diabetes history (or large child delivery >9lbs)
78
The ominous octet of type 2 diabetes causes
- Liver overproducing sugar
- B cells not making enough insulin (exhaustion after making excess in early stages of resistance)
- a cells making too much glucagon
- Skeletal muscle not taking up glucose
- GI tract and incretin effect
- Neurotransmitter dysfunction in the brain causing hunger
- Increased glucose reabsorption at the kidney
- increased lipolysis of fat cells
79
Metformin acts as a insulin ___ allowing the body to utilize its own insulin better
sensitizer
80
Metformin should be avoided when GFR is less than...
...45ml/min
81
When B cells fail and become ineffective at producing insulin, what happens to sulfonylureas?
They lose functionality only facilitate secretion of insulin
82
Meglitinides (name 2 examples) vs sulfonylureas
Meglitinides (repaglinide and nateglinide) are rapid onset oral agents for diabetes to stimulate insulin release and short duration taken with each meal and are not sulfa derivatives and are also safe with renal insufficiency, but like sulfonylureas are not effective with B cell failure
83
Pioglitazone function and ADR's/contraindications (1)
- Insulin sensitizer drug that is also very good at increasing HDL
- leads to weight gain due to edema (contraindicated in congestive heart failure patients)
84
The incretin effect
Refers to how GLP-1 is secreted upon ingestion of food entering the small intestine which enhances insulin secretion from the B cells dependent on the glucose levels as well as decreases excess glucagon (reducing strain on liver) and turns off appetite urges. This prolongs lifespan and health of B cells.
GLP-1 is not or very little secreted in type 2 diabetics, so GLP-1 agonists that tweak the molecule to lengthen its very short half life allow for injection once a week
85
DPP-4 inhibitors work at the incretin system by...
...blocking breakdown of patient's own incretin hormones raising their own GLP-1 levels several fold in type 2 diabetics
86
SGLT2 inhibitors action
Typically 100% of glucose is filtered into the nephron, but at the proximal tubule almost all absorbed along Na+ by SGLT2 transporter, can allow for urination out of about 100grams/day of glucose (weight loss and calorie loss as well), this also lowers blood pressure by dragging fluid with because we are losing glucose and sodium, worry is entering diabetic ketoacidosis
87
SGLT2 inhibitors demonstrate reduction in...
...Reduction in cardiovascular death, MI, stroke, and all cause mortality in all patients with type 2 diabetes (this is rare and big! Even cardiologists are using this in patients without diabetes, and are also renal protective in patients with type 2 diabetes OVER ACEI's and ARBs)
88
4 benefits of SGLT2 inhibitors and list the 4 agents
- Diabetes treatment
- Weight reduction
- Cardiovascular disease protection
- Renal protection
-Ivokana, farxiga, jardiance, steglatro
89
Insulin mixtures ending in -lin vs -log
Lin corresponds to rapid acting component being regular insulin (works within 30 min), log correspodns to rapid acting component being humalog (acts within 15 min)
90
Hypoglycemia definition
Episode of abnormally low plasma glucose conc. that exposes an indiviual to potential harm, considered severe (uncorrectable by self) when <70mg/dL
91
Symptoms of hypoglycemia (7)
- palpitations
- tremor
- sweating
- hunger
- paresthesia
- cognitive or behavioral change
- more than 50% asymptomatic***
92
If a patient is on metformin, sulfonylurea, and SGLT2 all to control diabetes and they have a hypoglycemic episode, the culprit of their reaction and the one to lower is the...
....sulfonylurea
93
Hypoglycemia treatment in a patient who can still consume food
- 2-3 glucose tabs
- 3-5 hard candies
- etc.
- Repeat if not improved in 15 minutes
- follow with meal of bread and protein
94
Medication adjustment for hypoglycemic episode should only be considered when not readily explained by...
....conventional factors including skipped or irregular meals or unaccustomed exercise
95
Neovascularization of the retina
The body's response to lack of adequate blood flow due to hypoglycemia to the retina by making new vessels that are very fragile and can leak exudates blocking vision
96
Metabolic memory/legacy effect
Refers to how patients who have early aggressive management of diabetes have better outcomes and less progression in retinopathy, neuropathy, and nephropathy than those who did not even after returning to less intense therapy later on
97
Diabetic retinopathy treatment (2)
- Panretinal laser photocoagulation decreases loss in patients
- Focal laser photocoagulation in eyes decreases loss in patients
98
Earliest marker of diabetic nephropathy we should test for in at risk groups for diabetes progression
Microalbuminuria (more predictive as can detect lower levels than a dipstick and progression is likelty to result in end stage renal disease)
99
Diabetic nephropathy albuminuria requires ___ abnormal specimens over __ time period to make diagnosis
2-3, 3-6 months
100
Even in the absence of hypertension, if a patient has presence of micro or macroalbumin they should be placed on...
....an ACEI or ARB (never both just FYI)
101
Recall, ACEI and ARB's dilate what vessel of the renal system?
Efferent arteriole
102
SGLT2 inhibitors constrict what vessel of the renal system?
Afferent arterioles
103
Common presentation of diabetic peripheral neuropathy
Chronic, symmetrical**, length dependent (feet before hands) sensation then motor polyneuropathy with nocturnal exacerbation making prickly pain worse
104
Thyroid disease epidemiology
- Most autoimmune
- Women>men
- Familial predisposition
- Radiation exposure risk
105
Drug effects on the thyroid
- Estrogen therapy increases thyroid binding and thus may require increased dosing of thyroid hormone to maintain free hormone levels
- Biotin in popular supplements can interfere with lab testing (hold 48 hrs before testing)
- supplements such as antacids can prevent absorption of thyroid hormone
106
Differential for hyperthyroidism causes (5)
- Graves disease
- Toxic multinodular goiter
- Toxic adenoma
- Subacute thyroiditis
- Iatrogenic origin
107
Common presentation of hyperthyroidism (4)
- Sweating, tremor, palpitations
- widened pulse pressure and tachycardia
- proximal muscle weakness
- lid lag
108
Graves disease
Most common hyperthyroid disease onset of 20-50 years of age where an individual has developed autoantibodies for the TSH receptor at the thyroid causing excessive thyroid activity
109
Graves opthalmopathy
Immunologic mediated accumulation of extracellular water and ground substance that only occurs in about 20% of patients with graves disease unless they smoke which greatly increases risk, can result in diplopia or vision loss (optic nerve can stretch out causing everything to get green hue)
110
Lab results (TSH, free T3/4, thyrotropin receptor antibody test) in Graves disease
- TSH low
- T3/4 elevated
- Positive thyrotropin receptor antibody test
111
Hyperthyroidism from Graves disease treatment options (5) and ADR (1)
- Antithyroid drugs tapazole and PTU (block production of thyroid hormone), B blockers to control side effects, irradiation therapy, surgery
- Agranulocytosis (leukopenia)
112
Why is tapazole preferred to PTU for treatment of hyperthyroidism?
-It is not as hepatotoxic, but preference is reversed in pregnancy
113
Subacute thyroiditis progression
- Initial phase of hyperthyroidism from healthy stores of thyroid hormone being released due to viral mediation
- Later transient phase of hypothyroidism
- Total resolution by 2-3 months
114
Subacute thyroiditis treatment options (4)
- Analgesics/NSAIDs
- B blocker in hyperthyroid phase
- thyroid hormone if hypothyroid phase
- Self limiting and does not return
115
Presentation of new onset of afib in elderly indicates need for...
....thyroid studies
116
Peroxidase antibody
Test for hypothyroidism, if positive usually indicates hashimoto's hypothyroidism
117
Hypothyroidism treatment options (1)
-Synthroid (L thyroxine)
118
Amiodarone and thyroid function
Can cause toxic effect on thyroid cell due to high iodine content, usually in a patient with underling hashimoto's hypothyroidism and thus has the same signs and symptoms or hyperthyroidism either type I (excess iodine) or type II (destructive thyroiditis)
119
Lithium and thyroid function and treatment (1)
Taken up by thyroid cells but cannot be utilized and thus inhibits formation and secretion of T3/4, changes in patients with underlying hashimoto's hypothyroidism (goiter, fatigue), treated with supplemental synthroid
120
Postpartum thyroiditis
Presents like hyperthyroidism in the setting of postpartum approx 4-7% of population due to inflammation causing same course as subacute thyroiditis (hyperthyroid phase that is severe and looks like graves but lacks thyroid stimulating immunoglobin levels and gets better with time followed by hypothyroid phase)
121
Postpartum thyroiditis treatment options (3)
- Self limiting and recurs with future pregnancy***
- B blockers for hyperthyroid phase
- Thyroid replacement for hypothyroid phase
122
Hyperthyroidism treatment of choice in pregnant woman with graves disease
-PTU (does cross placenta, need to give lowest amount to keep mother's levels normal)
123
Thyroid cancer frequency, diagnostic tests (2)
-only 5% of nodules are cancer (relatively rare), ultrasound determine solid vs cyst and size (<1cm no clinical significance) and regular border no concern or fine needle aspiration
124
Hot vs cold nodules (thyroid scan)
Hot have high radiologic activity and cold do not, cold are more concerning for cancer
125
Most common type of thyroid cancer and management (5)
- Papillary
- Resection of gland, iodine ablation, thyroid hormone replacement, whole body scan, serum thyroglobulin (only present if not all thyroid tissue was removed)
126
Sick euthyroid syndrome
Acute or chronic non-thyroidal illness that is often seen with decreased T3/4 with normal TSH and has no thyroid treatment necessary
127
Role of parathyroid hormone
Maintain extracellular fluid ca2+ balance, acts directly on bone and kidney, acts indirectly on gut thru vit d production
128
Differential for hypercalcemia (6)
- PTH related
- Malignancy
- Vit D intoxication
- Hyperthyroidism
- thiazide diuretics
- Excessive alkaline agent ingestion
129
Hypercalcemia clinical features (4)
- asymptomatic
- fatigue, depression
- N/V
- stone formation
130
Primary hyperparathyroidism
Inappropriate elevation of PTH levels in relation to elevated Ca2+ levels, most often caused by a solitary adenoma
131
Treatment indications for primary hyperparathyroidism in asymptomatic patients (4)
- Only if serum Ca2+ >1.0mg/dL above normal
- or if osteoporosis development
- or if age less than 50
- or if kidney impairment
132
Treatment for primary hyperparathyroidism first choice and backup option
- Surgical removal using intraoperative rapid PTH assays between removing one parathyroid gland or in the case of 4 gland hyperplasia remove 3.5 glands and autotransplant remnant into forearm
- Cinacalcet (sensipar) that is a calcimimetic agent that lowers PTH levels
133
Chvostek sign
Light tap on facial nerve sees corner of mouth twitch in response, common in normal individuals but bilateral can indicate hypocalcemia
134
Trousseau's sign
Pump blood pressure cuff above systolic and retain it until the patient cramps up due to acidosis, indicative of hypocalcemia
135
Differential for hypocalcemia (4)
- chronic renal failure
- hypoparathyroidism
- vit D deficiency
- transient
136
Hypocalcemia signs and symptoms (3)
- muscle spasms, convulsions
- mental status change
- positive chvostek and trousseau sign
137
Vit D action
Increases intestinal ca2+ absorption and increases effect of PTH on the bone, sourced from sunlight or from fortified foods, converted to active form at liver and kidney and acts on gut
138
Common causes of vit D deficiency (3)
- GI malabsorption
- Cirrhosis or kidney failure
- steroids/anticonvulsants
139
Vitamin D replacement therapy
Vit D3 50,000 IU weekly for 4-6 weeks, then maintenance 800-2000 IU daily
140
Cushing's syndrome and different sources
Adrenal hyperplasia causing excess cortisol production
-pituitary hyperplasia, pituitary ACTH overproduction, ectopic ACTH production from a tumor producing a similar substance, adrenal adenoma, adrenal cancer, or prolonged use of steroids
141
Cushing's syndrome screening tests (3)
- Overnight dexamethasone suppression test (administer 1mg PO 11pm, serum cortisol next day taken at 8am, should suppress to <2ug/dL in healthy patient, abnormal >10ug/dL)
- 24 hr urine free cortisol measure (normal less than 50-75 ug in 24 hrs)
- late night salivary cortisol
142
Lesion location in confirmed screening cushing's syndrome
Radiographic studies to confirm suspicion? (3)
- ACTH and cortisol both high (pituitary or ectopic ACTH)
- ACTH low and cortisol high (indicates adrenal or iatrogenic origin)
- Pituitary MRI (only 50% accurate)
- Petrosal venous sinus sampling
- Abdominal CT or MRI's
143
Addison's disease
Chronically low cortisol levels due to primary adrenalcortical deficiency that progresses to destroy greater than 90% of the adrenal mass and may be associated with other endocrine autoimmune diseases, ACTH buildup in body darkens skin patches
144
Addison's disease presenting signs and symptoms (5)
- Fatigue, weakness, anorexia
- N/V
- Pigmentation of skin
- hypotension
- hypoglycemia
145
Lab evaluation of addison's disease
- Hyperkalemia and hyponatremia
- <10ug/dL serum AM cortisol
- ACTH stimulation test
146
ACTH stimulation test
Test for evaluation of Addison's disease where .25 mg ACTH IV or IM administered and then ACTH, cortisol, and aldosterone levels at 30, 60, and 90 min are compared to baseline value, normal to see >18-20 ug/dL during test, otherwise is abnormal response indicative of addison's dz
147
Adrenal insufficiency treatment options (2)
- Daily hydrocortisone 20mg in AM, 10mg in late afternoon
- - fludrocortisone (aldosterone agonist) .1mg per day with salt
148
Increasing daily hydrocortisone doze in adrenal insufficiency or illness/surgery recovery treatment adjustment scale
- Increase when sick or stressed using 3x3 rule (3x usual daily dose for 3 days)
149
Treatment for secondary adrenal insufficiency (2nd to previous high dose prolonged use of potent exoogenous steroids causing chronic ACTH suppression)
-20mg/day of prednisone for >3 weeks (high dose, long period of time)
150
Primary hyperaldosteronism causes (2)
-Either due to a solitary adenoma (bump on one adrenal gland making excess aldosterone that can be removed via surgery) or bilateral idiopathic hyperplasia (familial inheritance, treated with sprionolactone)
151
Primay hyperaldosteronism clinical features (3)
- Particularly severe hypertension
- Low serum K+
- Muscle weakness and polyuria
152
Primary hyperaldosteronism diagnostic criteria
- Hypertension
- hypokalemia
- Aldosterone/renin ratio (>30 is primary hyperaldosteronism, <10 is secondary hyperaldosteronism)
153
Drug of choice for bilateral hyperplasia treatment of primary hyperaldosteronism
Spironolactone 100mg/day
154
Pheochromocytoma
Life threatening tumor in the adrenal medulla where catecholamines are secreted that sees marked elevation in hypertension with paroxysms, 80% of the time in one adrenal gland EXCEPT in case of familial inheritance when seen bilateral
155
Pheochromocytoma labs (4) and which is the gold standard?
- Free catecholamines
- 24 hr urine preferable***
- Metanephrines
- Urinary VMA (both these are biproducts)
156
Pheochromocytoma management (5)
- a blocker then
- B blocker
- Enzyme blocker (block production of excess catecholamines)
- Localization with CT/MRI
- Surgery
157
Management of adrenal incidentaloma (2)
- Surgical in clincical functioning masses
- - Nonfunctioning may be benign and can be left in place
158
Prolactin is the only hormone without...
....a negative feedback loop (instead inhibited by dopamine)
159
Pituitary tumor characteristics (4)
- 1/3 nonfunctional (not secreting)
- Most produce one solitary hormone in excess
- Bitemporal hemianopsia (tumor forms at optic chiasm)
- Visual field exam (loss of peripheral vision)
160
Sheehan's syndrome
Post partum pituitary apoplexy (bleeding into and impaired blood supply to the pituitary) and infarction
161
Hyperprolactinemia causes (5)
- pregnancy (peak at delivery)
- nipple stimulation
- stress
- Prolactinoma
- chest wall injury
162
Why are men more susceptible to larger prolactinomas than females?
Men don't have the associated symptoms regarding amenorrhea and galactorrhea while females do much earlier on
163
Prolactinoma is the only tumor that the preferred method of treatment is...
....medication - dopamine agonists (bromocriptine or cabergoline)
164
Acromegaly
Condition caused by excess growth hormone from pituitary, slow gradual change in appearance of patient from symptoms to diagnosis for up to 12 years, both GH and IGF-1 increased, excess GH secretion making IGF-1 elevated
165
Best study for acromegaly diagnosis and why + one other
- IGF-1 (no diurnal variation)
- - MRI of pituitary (adenoma in almost 95% of causes)
166
Acromegaly treatment options (2)
- Transphenoidal surgery
- - Medical therapy
167
Diabetes insipidus
A deficiency of ADH second to many things including trauma, neoplasm, infection, etc. that results in large volumes of dilute urine and polydipsia
168
Diabetes insipidus diagnostic lab evaluation (2)
- 24 hr urine output >50ml/kg
- fluid deprivation test
169
Diabetes insipidus treatment (1)
Desmopressin (dDAVP) intranasal, oral, or subQ twice a day
170
Syndrome of inappropriate ADH and treatment (2)
Release of excess ADH causing retention and dilution of body fluids (eventually reaching hyponatremia), treated by restricting fluid and taking demeclocycline
