Review Part 2 Flashcards
1
Q
What are the clinical presentations of hyperthyroidism?
A
- Weight Loss
- Palpitations
- Diarrhea
- Tachycardia
- A. Fib
- Bounding Pulse
- Polyuria
- Heat Intolerance
2
Q
What are the labs/lab results used to dx hyperthyroidism?
A
- TSH: ↓
- TH (T4): ↑
3
Q
What are the clinical presentations of hypothyroidism?
A
- Dryness
- Constipation
- Bradycardia
- Dyspnea
- Peripheral Edema
- Delayed DTR’s
4
Q
What are the labs/lab results used to dx primary and secondary/tertiary hypothyroidism?
A
Primary: - TSH: ↑ - TH (T4): ↓ Secondary or tertiary: will decrease together - TSH: Normal to ↓ - TH (T4): ↓
5
Q
What are the clinical presentations of Myxedema coma crisis?
A
- Hypotension
- Reduces LOC
- Seizures
- Hypothermia
- Macroglossia
- Ptosis
6
Q
What are the labs/lab results used to dx Myxedema coma crisis?
A
- TSH:↑
- TH (T4): ↓
7
Q
What are the clinical presentations of Graves disease?
A
- Hyperthyroid symptoms
- Exophthalmos
- Dermatopathy
- Onycholysis
8
Q
What are the labs/lab results used to dx Graves disease?
A
- TSH: ↓
- TH (T4): ↑
9
Q
What are the clinical presentations of Subacute thyroiditis?
A
- Onset acute & severe
- Sore Throat
- Exquisitely tender, Enlarged gland (sm goiter)
- Febrile
- Signs of: hyper then hypo
10
Q
What are the labs/lab results used to dx Subacute thyroiditis?
A
- Thyroid function x 6 mo.
- WBC: ↑ (left shift)
- ESR: ↑
- FNA Bx: if in doubt
- TPO Ab: Negative
11
Q
What are the clinical presentations of Thyrotoxicosis/ Thyroid storm?
A
- Fever
- Vomiting
- Delirium
- Diarrhea
- Seizures/Coma
- Jaundice
12
Q
What are the labs/lab results used to dx Thyrotoxicosis/ Thyroid storm?
A
- TSH: ↓
- TH (T4): ↑
13
Q
What is adrenarche?
A
Onset of androgen-dependent body changes such as growth of axillary and pubic hair, body odor, and acne
14
Q
What is acral?
A
Pertaining to peripheral body parts, such as toes and fingers
15
Q
What is acanthosis nigricans?
A
- Common skin pigmentation disorder
- Dark patches of skin with a thick, velvety texture
16
Q
What is amenorrhea?
A
Absence of menstruation
17
Q
What is exopthalmosis?
A
- Prominence of eyes
- “bulging eyes”
18
Q
What is proptosis?
A
Abnormal protrusion or displacement of an eye or other body due to all other causes
19
Q
What is hirsutism?
A
Condition of male-pattern hair growth in women
20
Q
What is menarche?
A
Onset of menstruation
21
Q
What is precocious puberty?
A
Onset of puberty at an abnormally early age
22
Q
What is puberty?
A
Appearance of sexual hair
23
Q
What is striae?
A
Irregular areas of skin that look like bands, stripes or lines
24
Q
What is thelarche?
A
Onset of female breast development
25
What is virilization?
Biological development of sex differences
26
What is acromegaly?
- Abnormal growth of hands, feet, jaw and face.
- D/t overproduction of GH in adulthood
- Does not grow linear
27
What is dwarfism?
- GH deficiency
- Etiology: genetics
- Common complications: Bowing of legs, hunching of the back, and crowded teeth
28
What is disproportionate and proportionate dwarfism?
Disproportionate:
- Average size torso w/ shorter extremities or vice versa
Proportionate:
- Body parts are proportion but shortened
29
What is Galactorrhea?
- Discharge of milk-like substance from the breast
| - Caused by Hyperprolactinemia
30
What is an acrochordon and what diseases are these seen in?
- Skin tags
- Common in DM pts
- If in younger pts think Cushing's disease
31
What is the workup for possible DM?
- Screen all adults over 45 yrs q 3 yrs
- At least 1 risk factors (obesity, family hx, hx of gestational dm) + BMI >25
- Early screening for AA and Native Americans
32
What is the MC cause of SIADH?
ADH producing tumors: SCLC
33
What is the clinical presentation of SIADH?
- Hyponatremia sxs
- Weakness
- HA
- Weight gain
- N/V
- Coma
- Mental status change
- Seizures
- Irritability
34
What are the complications of SIADH?
- Hyponatremia
- Hypo-osmolality
- Increase in water retention and impaired water excretion
- Loss of or dilution of electrolytes or solutes (Na, K, Cl)
35
What are the dx test for SIADH?
- CBC: H&H ↓
- CMP: BUN/Cr ↓ and electrolytes (Na, K, Cl): ↓
- Plasma Cortisol: ↓
- ADH: ↑
- CT scan of head and CXR: Meningitis, Tumor mass, Neoplasm, Infectious process
- Radioimmunoassay of ADH
36
What is the management of SIADH?
- Treat underlying cause
- Fluid restriction of 800-1,000 ml/d
- IV saline for symptomatic pts only (confusion, convulsions, coma)
- TURF TURF TURF
37
What is the cause of DI?
- Kidneys are unable to prevent excretion of water
- ADH deficiency (pituitary and Neurogenic DI)
OR
- Unresponsiveness of renal tubules to ADH (Nephrogenic DI)
38
What are the causes of Neurogenic/pituitary DI?
- Idiopathic
- Neoplasm of brain of pituitary gland
- Head trauma: basal skull fx
- Granulomatous disorders: sarcoidosis or TB
- Meningitis
- Post encephalitis
- MS
- Guillain barre syndrome
39
What are the causes of Nephrogenic DI?
- Drugs: Lithium
- Metabolic: hypercalcemia and hypokalemia
- Sarcoidosis
- Sickle Cell disease
- Low protein diets
40
What is the presentation of DI?
- Abrupt onset
- Nocturia
- Polyuria: 2.5 - 6 L/day
- Polydipsia
- Neuro manifestations: Seizures, HA, visual field defects
41
What is the complication of DI?
Inability to concentrate urine
42
How do you diagnose DI?
- Vasopressin: differentiate between nephro and neuro DI. >50% increase of urine osmolarity = neurogenic
- Hypernatremia
- Urine and plasma osmolarity: >295 mOsm/kg
- MRI of pituitary gland
43
What is the management of DI?
Endocrinology consultation for dx testing, referral and structured tx plan
44
What are the functions of ADH?
- Regulate water retention in the kidneys
| - Vascular constriction
45
What are ADH deficiencies?
- Cause of DI
| - Increased thirst and frequent urination
46
What are EKG findings of hypocalcemia?
Prolonged QT interval
47
What are EKG findings for hypokalemia?
- Prominent U wave
| - T wave flattened
48
What are EKG findings of hyperkalemia?
- Tall peaked T waves
- QT interval shortened
- P wave flattening
49
What are EKG findings of hypomagnesemia?
- Torsades
- Prolonged PR and QT interval
- Afib
- Vfib
- Ventricular tachycardia
50
What are incidentalomas?
- Pituitary lesions that are discovered while investigating other neurological problems
- Not causing any physiological changes/associated symptoms
51
What is the cause of gigantism?
- Too much growth hormone as a child
| - Epiphyseal growth plates are open
52
What is the presentation of gigantism?
- Vertical growth
- Tall stature course facial features
- Enlarged forehead
- Large hands and feet
53
What are S/Sxs of a pituitary adenoma (peds lecture)?
- Vision changes and HA
| - Hormones can also be affected, interfering with menstrual cycles and causing sexual dysfunctions
54
What is the tx of a pituitary adenoma (peds lecture)?
- Surgery and Medication to block excess hormone production or shrink the tumor
- In some cases: radiation
55
What is precious puberty? and what age does it typically occur in girls and boys?
- Onset of puberty at an early age
- Girls: 8 yrs (may be 7 in AA, Mexican and American girls)
- Boys: 9 yrs
56
What are the labs/lab results used to dx central (true) precocious puberty?
- LH, FSH, testosterone, estradiol, DHEAS, Androstenedione: all elevated
- Refer!
57
What are the labs/lab results used to dx peripheral variety precocious puberty?
- Low gonadotropins and various steroid results
| - Refer!
58
What pubertal changes are present that needs to be evaluated? which hormones are involved in each?
- Breast development: estrogen
- Body odor, pubic/axillary hair, skin changes (androgens)
- Boys: if androgen changes w/o testicular growth think exogenous testosterone
59
What is delayed puberty? and what age does it typically occur in girls and boys?
- Girls: no breast development by age 13 yrs
| - Boys: no testicular development (SMR 2) by age 14 yrs
60
What is the MC delayed puberty?
```
Constitutional delay
(more concerning compared to familial short structure)
```
61
What is constitutional delay?
- Puberty and height delay
- Bone age delay
- Often positive w/family hx
- Follow longitudinally, occasionally low dose short course testosterone in boys
62
What are the screening tests for delayed puberty?
- General health: CBC, CMP, thyroid
| - Gonadotropins: LH, FSH should be ↓
63
If levels of gonadotropin are increased what would that mean?
Gonad failure
64
What is Klinefelter syndrome? and what are the clinical presentations?
- Occurs in males (C.47, XXY)
- Small testes
- Sparse pubic, armpit, and facial hair
- Enlarged breast
- Tall stature
65
What are the lab findings in a pt w/ Klinefelter syndrome?
- LH and FSH: ↑
| - Testosterone: ↓
66
What is Turner syndrome? and what are the clinical presentations?
- Occurs in Females (C.45, XY)
| - webbed neck, lymphedema nevi (brown spots), short stature
67
What are the lab findings in a pt w/ Turner syndrome?
- LH and FSH: ↑
| - Estrogen: ↓
68
What is tanner staging (I-V)?
- I: flat, alONE --> no pubic hair
- II: 11 yrs old, 2 breast buds form, pubic hair appear, 2 balls (teste enlargement)
- III: 13 yrs old, breast mounds form, course, curly pubic hair, penis increases in size and testicular growth
- IV: 14 yrs old, coarse pubic hair, not on thighs yet, raised alveolar, 2 mounds form
- V: adult, pubic hair extends onto thighs
69
When does tanner staging usually start? and what stage is the 1 sign of puberty?
- 10 yrs old
| - Tanner stage II is the 1st sign of puberty
70
What is Prader-Wili syndrome?
- Hypogonadotropic hypogonadism
- Prenatal hypotonia
- Postnatal growth delay
- Development disabilities
- Obesity after infancy
71
What are early childhood sings of Prader-Wili syndrome?
- Constantly hungry
- Hyperphagia
- Obesity
72
What does Prader-Wili syndrome cause in adolescent children?
- Premature development and axillary hair w/delay of the other secondary sex characteristics
- Increased incidence of epilepsy and scoliosis
73
What are the physical characteristics of Prader-Wili syndrome?
- Almond-shaped eyes
- High/narrow forehead
- Thin upper lip w/ small, downturned mouth
- Prominent nasal bridge
- Small feet and hands
- Soft skin
- Excess fat
74
What is the onset, age, body type in type 1 DM? and is ketosis common or rare?
- Sudden onset
- Any age, typically young
- Usually thin
- Ketosis is common
75
What is the classic triad of DM1?
- Polyuria
- Polydipsia
- Weight loss
76
What is the onset, age, body type in type 2 DM? and is ketosis common or rare?
- Gradual onset
- Onset of age mostly in adults
- Frequently obese
- Ketosis is rare
77
Why is there usually no sxs in a pt with congenital hypothyroidism?
Usually no sxs at birth d/t having moms TSH level in utero
78
What are early signs of congenital hypothyroidism?
- Decreased activity, tone, and temp
- Prolonged jaundice
- Large fontanelles
- Puffy hands
- Protuberant abdomen
79
What are late signs of congenital hypothyroidism?
- Poor growth
- Lethargy
- Mottling
- Breathing difficulty
- Edema
- Umbilical hernia
- Developmental delay
80
What lab test should be performed for congenital hypothyroidism? and how do you treat?
- TSH, if elevated get T4 and T3
| - Begin Levothyroxine as soon as dx is confirmed (early brain damage is irreversible)
81
Aside from labs what are other workups that can be done for congenital hypothyroidism?
- Radioactive iodine test to look for absent or ectopic thyroid gland
- May see a goiter: defects in synthesis
- Check iodine levels (severe iodine deficiency should be seen)
82
What is primary hypogonadism?
Ovaries or testes themselves do not function properly
83
What is central hypogonadism?
Centers in the brain that control the gonads (hypothalamus and pituitary) do not function properly
84
What can you expect to see in girls (pre-puberty) with hypogonadism?
- Will not begin menstruating
| - Will affect breast development and height
85
What can you expect to see in women with hypogonadism?
- Hot flashes
- Loss of body hair
- Low libido
- Menstruation stops
86
What can you expect to see in boys (pre-puberty) with hypogonadism?
- Lack of muscle and beard development
| - Growth problems
87
What can you expect to see in men with hypogonadism?
- Breast enlargement
- Decrease beard and body hair
- Muscle loss
- Sexual problems
88
What is the first line oral tx for DM2? (class name and drug name)
Bigunaides: Metformin
89
What is the MOA of Metformin?
- Reduces hepatic resistance to insulin and decreases hepatic glucose dumping
- Insulin sensitizers in the liver
90
What are the ASEs of Metformin?
GI distress:
- Nausea
- Diarrhea
- Abdominal pain
91
How do you improve GI distress caused by metformin?
- Slow dose- titration
- Administration w/after a meal
- ER formulations
92
Metformin is primarily eliminated by what? and is CI in pts with what?
- The kidneys
| - Impaired renal fxn or acute/unstable HF d/t concern of lactic acidosis
93
What eGFR levels do you not want to start Metformin? What eGFR levels do you want to d/c Metformin in a pt whos been taking it for a while?
- Don't start: <45
| - Discontinue: <30
94
What other drug is apart of the Biguanides class? and why was it withdrawn?
- Phenformin
| - High rates of mortality and lactic acidosis
95
What line of tx is Sodium-GLucose Transporter-2 (SGLT-2) Inhibitors? and how are they excreted?
- 2nd line tx
| - Renal
96
What are the drug names in the SGLT-2 class?
"-gliflozin"
- Canagliflozin
- Dapagliflozin
- Empagliflozin
- Ertugliflozin
97
What is the MOA of SGLT-2?
- Reduce blood sugar by increasing urinary glucose excretion.
- Reabsorption of glucose (co-transported with sodium) occurs in the proximal tubule via the SGLT.
98
Which SGLT-2 is usually added to monotherapy that shows better lower A1c effect as well as better effects on weight and hypoglycemia?
Canagliflozin + Metformin
99
What are the "advantages" of SGLT-2 drugs?
- Reduce CV (HF) and renal events
- Lower A1c
- Low risk of hypoglycemia
- Lower B/P (↓ systolic by 3-5 mmHg)
100
SGLT-2 drugs are eliminated by what? and is CI in pts with what?
- The kidneys
| - Severe renal impairment
101
What are the ASEs/Warnings of SGLT-2 drugs?
- GU infxns (UTI and candida)
- Euglycemia DKA
- Amputation
- Fournier gangrene
- Fracture risk
- $$$
102
What line of tx are the Thiazolidinediones? are eliminated by what?
- 3rd line
| - Hepatic
103
What are the drug names in the Thiazolidinedione class?
- Pioglitazone
| - Rosiglitazone
104
What is the MOA of the Thiazolidinedione drugs?
- Agonism of the PPAR-y receptor
- Insulin sensitizers in the peripheral insulin-responsive tissues
- Receptor located primarily in adipose tissue
105
What is the rate of glycemic control of the Thiazolidinedione drugs?
Slow, occurs over wks to months as tissue insulin-sensitive improves and FFA levels are reduced
106
Why was the drug Troglitazone (Thiazolidinedione) withdrawn from the market?
Rare but severe liver toxicity
107
What is the concern of Rosiglitazone?
MI risks
108
What is the concern of Pioglitazone?
Risk for bladder cancer
109
What are the ASEs of the Thiazolidinedione class?
- Water retention and weight gain
- Macular edema
- Anemia
- Bone density loss (osteoporosis)
- Increase fracture risk
- Monitor liver enzymes
110
What is the BBW and CI of Thiazolidinediones?
- BBW: may cause of exacerbate CHF
| - CI: CHF, hepatocellular disease, and pts with ALT >2.5x the norm
111
What line of tx are the GLP-1 Analogs? are eliminated by what?
- 2nd line
| - Renal
112
What are the drugs in the GLP-1 Analog class?
- Exenatide
- Liraglutide
- Dulaglutide
- Semaglutide
113
What is the MOA of GLP-1 Analog class?
- Stimulates insulin synthesis and release
- Suppress post-prandial glucagon secretion
- Slows gastric emptying and has an anorectic effect.
114
Are almost all GLP-1 SubQ or oral? What is unique about Semaglutide?
- SubQ ( most often used in addition to oral diabetes meds, but can be added to basal insulin)
- Semaglutide is the only oral
115
What are common ASEs and the serious ASEs of GLP-1 Analogs?
```
Common:
- Nausea (MC)
- HA
- Infxn
Serious:
- Pancreatitis
- Immunolocis rxns
- Acute kidney injury
- Angioedema
```
116
What is the BBW and CI of GLP-1 Analogs?
- BBW: Thyroid c-cell tumor
| - CI: Personal and family hx of medullary thyroid carcinoma and in pts w/ MEN 2
117
How often is Liraglutide (Victoza) administered? and when added to Metformin it improves what?
- SubQ once daily
| - Improve outcomes in pts w/ established ASCVD
118
Liraglutide (Saxenda) is often used as an adjunct to reduce what?
Reduce calorie diet and increase physical activity for chronic weight management in adult pts w/ obesity or overweight + weight-related comorbidity
119
What drug is a new once weakly GLP-1 agonist?
Extenatide ER
120
GLP-1 agonist are primarily combined with other medications except for what drug class?
DPP-4 inhibitors (d/t MOA)
121
What line of tx are the Dipeptidyl Peptidase-4 (DPP-4) Inhibitors? are eliminated by what?
- 2nd line
| - Most are renal excreted but Linagliptin is most excreted by bile
122
What are the drugs in the DPP-4 Inhibitor class?
"-liptin" (like Lipton tea)
- Sitagliptin
- Saxagliptin
- Linagliptin
- Alogliptin
123
What is the MOA of DPP-4 Inhibitors?
Increase GLP-1 concentrations by inhibiting the enzyme that metabolizes endogenous GLP-1, dipeptidyl peptidase-4 (DPP-4)
124
What are the advantages of DPP-4 inhibitors? and what med are these usually combined with?
- Oral administration
- weight neutral
- combined with metformin (A1c lowering 1.5-2%)
125
What is the increased risk when combining DDP-4 + SU?
Hypoglycemia
126
What line of tx are the a-Glucosidase inhibitors? and are eliminated by what?
- 3rd line
| - Renal and bile (50%)
127
What are the drugs in the a-Glucosidase inhibitor class?
- Acarbose
| - Miglitol
128
What is the MOA of a-Glucosidase inhibitors?
Inhibits a-glucosidase and delays/reduces absorption of dietary carbohydrate given before carbohydrate load
129
What are the ASEs of a-Glucosidase inhibitors?
- Flatulence
- Diarrhea
- Abdominal pain
130
What line of tx is the bile acid sequestrant? are eliminated by what?
- 3rd line
| - Bile
131
What is the only drug in the bile acid sequestrant class?
Colesevlam
132
Colesevlam is useful in treating pts with DM type 2 and what?
Dyslipidemia.
133
When taking Colesevlam with meals it can cause what?
- Can bind other drugs
- Increase serum triglycerides
- Cause constipation or bloating.
134
Why would a pt not want to take Colesevlam?
- Large tablets and need to take many per day.
| - Dose = 3 tabs BID or 6 tabs QD with meals
135
What line of tx are Sulfonylureas 2nd gen? are eliminated by what?
- 2nd line
| - Hepatic
136
What are the drugs in the Sulfonylureas 2nd gen class?
- Glipizide
- Glimepiride
- Glyburide
137
What is the MOA of the Sulfonylureas 2nd gen class?
Binds to SUR1, closes the ATP-sensitive K channel and causes B-cell depolarization and insulin exocytosis
138
What are the ASEs and CI of Sulfonylureas 2nd gen class?
- ASEs: hypoglycemia and nocturnal hypoglycemia
| - CI: pts w/ sulfa allergies
139
What drug of the Sulfonylureas 2nd gen class is the most potent?
Glyburide
| -causes 2x more hypoglycemia than Glipizide or Glimepiride
140
What line of tx are the other Secretagogues/Meglitinides? and eliminated by what?
- 2nd line
| - Hepatic
141
What are the dugs in the Secretagogues/Meglitinides class?
- Repaglinide
| - Nateglinide
142
What is the MOA of the Secretagogues/Meglitinides class?
Short-acting, closes ATP-sensitive K channel to stimulate insulin release
143
What is the benefits/indications of drugs in the Secretagogues/Meglitinides class?
- Postprandial glucose excursions
- No sulfa group
- Simply hold a dose if missed a meal
144
Why wouldn't a pt want to take drug from the Secretagogues/Meglitinides class?
- Multiple doses per day; 3-4
| - $$$
145
What is good DM control?
- Healthy diet and exercise routine
- A1c goal <7.0%
- Fasting glucose: 80 - 130
- Postprandial glucose: <180
146
What is the setting for use of rapid insulin?
- Post-prandial glucose peaks
- Usually combined with long acting
- Preferred for insulin pumps
147
What is the setting for use of short insulin?
Covers insulin needs for meals eaten within 30-60 minutes
148
What is the setting for use of intermediate insulin?
- Covers insulin need for about half the day or overnight
| - Often combined with a rapid or short-acting insulin
149
What is the setting for use of long insulin?
- Covers insulin needs for about a day
| - Often combined when needed with rapid or short-acting insulin
150
What is the typical DM type 1 insulin tx?
Long-acting (basal) insulin and rapid/short-acting insulin at mealtimes
151
What is the typical DM type 2 insulin tx?
Long-acting (basal) insulin (esp. when adding to oral agents), prandial insulin is optional and often helpful
152
What is the indication for glucagon?
SubQ injected glucagon is the preferred tx of hypoglycemia for an unconscious pt
153
When to you use oral glucose?
- Oral glucose dose 15 g is the preferred treatment of conscious hypoglycemic pt
- Monitor blood glucose to ensure adequate tx
- Repeat dose if necessary after 15 minutes
154
What is the 1st line tx for Hypothyroidism?
Levothyroxine (T4)
155
What is the MOA of Levothyroxine (T4)?
A synthetic form of thyroxine (T4), converts to its active metabolite triiodothyronine (T3)
156
What are the other indications of Levothyroxine (T4)?
- Hypothyroidism
- Postpartum thyroiditis
- Subacute de Quervain's Painful Thyroiditis
- Myxedema Coma
- TSH Suppression for thyroid cancer
157
What is the dosing adjustment of Levothyroxine (T4) for pregnancy? and in general when should it be taken?
- Frequent increase during pregnancy: increase by 30-50%
| - Should be taken first thing in the morning at least 30-60 minutes before breakfast
158
What is the dosing of Levothyroxine (T4) in adults and elderly?
- Adults <60 w/o CAD: 50-100 ug daily
| - Elderly or known CAD: 12.5-25 ug daily
159
What are the ASEs and CI of Levothyroxine (T4)?
- ASEs: can alter INR and interact with drugs that bind to the GI (Sucralfate and Bile Acid Sequestrants)
- CIs: for tx of obesity or weight loss
160
What is the medication for T3 and indication?
- Liothyronine
- Used in combination w/ levothyroxine for pts who don’t get adequate T4 to T3 conversion
- Antidepressant augmentation (rarely)
161
What are ASEs and CIs of Liothyronine?
ASEs:
- Tachycardia
- Angina
- Tremors
- Can alter INR and interact with drugs that bind to the GI
CIs:
- should not be used on its own for thyroid supplementation and do not use for weight loss
162
What is the thyroid medication that has both T3 and T4?
Desiccated Porcine Thyroid
163
What is the MOA of Desiccated Porcine Thyroid? and indication?
- MOA: T3 converted to T4
| - Indication: Hypothyroidism
164
What is the ASEs of Desiccated Porcine Thyroid?
ASEs:
- Tachycardia
- Angina
- Tremors
- Can alter INR and interact with drugs that bind to the GI
165
What is the drug class and drugs used for hyperthyroidism?
- Thyroid Synthesis Inhibitors
| - Propylthiouracil (PTU) and Methimazole
166
What is the MOA of PTU?
inhibits the synthesis of TH by interfering w/ thyroid peroxidase TPO
167
What are the indications of PTU?
- Hyperthyroidism
| - Thyroid storm in pregnant women
168
What is the dosing of PTU? and how long does it take to reach full benefit?
- TID dosing
| - Full benefit may take 6-12 mos
169
What are the ASEs and CIs of PTU?
ASES:
- Agranulocytosis
- Not always able to establish a euthyroid state: may lead to hypothyroidism
- Concerns in pregnancy and lactation (Cat. D)
- Can cause severe liver damage
170
What is the BBW of PTU?
- Only use during or just prior to the first trimester
| - Impaired liver dz
171
What is the MOA of Methimazole?
Inhibits the synthesis of thyroid hormones by blocking the oxidation of iodine in the thyroid gland
172
What are the indications of Methimazole?
- Hyperthyroidism
- May be used as adjunct therapy to thyroid irradiation
- Used in place of PTU in impaired liver dz
173
What is the dosing of Methimazole? and how long does it take to reach full benefit?
- Once daily dosing
| - May take 3-12 weeks for euthyroid state
174
What are the ASEs and CI of Methimazole?
ASEs:
- More dangerous than PTU during 1st trimester of pregnancy and lactation. (Cat. D)
- Agranulocytosis
175
What is the BBW of Methimazole?
Only use Methimazole for 2nd and 3rd trimesters.
176
What is the clinical use of BBs in a pt with thyroid dz? and which BB is used?
- Propanolol
| - Used for symptomatic relied not for tx of hyperthyroidism
177
What symptoms does Propanolol help suppress?
- Tachycardia
- Tremor
- Anxiety
- Other sxs of hyperthyroidism
178
What is the low, moderate, and high potency glucocorticoid therapy?
- Low: Hydrocortisone
- Moderate: Prednisone
- High: Dexamethasone
179
What are the indications of Fludrocortisone?
- Provides additional mineralocorticoid support
- Prevents/treats: sodium loss, vascular volume depletion and hyperkalemia
(ie. blood pressure and electrolyte support in adrenal insufficiency)
180
What are the diseases that Fludrocortison is used to treat?
- Addison's disease
- Primary hypoaldosteronism
- Congenital adrenal hyperplasia
181
What are the ASEs of Fludrocortison?
- HTN
- Edema
- Cardiac enlargement
- Hypokalemia
