Internal Med- Endo + Neuro Flashcards
1
Q
25-year-old man concerned about some “bizarre symptoms” that he has been. He tells you that approximately 6 months ago, he began to experience the following symptoms: headaches, visual defects, weight gain, an appearance of his forehead growing, enlarging hands and feet (he could no longer get his gloves and shoes on), and increased sweating. On examination, mental status is normal, and the apical impulse is felt in the fifth intercostal space, midclavicular line. His blood pressure is 170/ 105 mm Hg. He does have a protruding brow, and three discrete visual field defects are noted (two in the left eye and one in the right eye). His tongue appears enlarged, and he is sweating profusely.
A
Acromegaly
2
Q
Etiology of acromegaly
A
pituitary adenoma that secretes excessive amounts of Growth Hormone; rarely, they are caused by non-pituitary tumors that secrete GHRH
3
Q
occurs if growth hormone (GH) hypersecretion begins in childhood, before the closure of the epiphyses
A
Gigantism
Acromegaly involves growth hormone GH hypersecretion beginning in adulthood; a variety of bony and soft tissue abnormalities develop
4
Q
Whats the difference in Acromegaly vs Gigantism
A
- Gigantism occurs if growth hormone (GH) hypersecretion begins in childhood, before the closure of the epiphyses
- Acromegaly involves growth hormone GH hypersecretion beginning in adulthood; a variety of bony and soft tissue abnormalities develop
5
Q
Dx studies for acromegaly
A
- GH test 2 hour after glucose load
- Increased IGF-1
- MRI/CT shows a pituitary tumor
6
Q
Tx of acromegaly
A
Pituitary tumor removal
7
Q
a 25-year-old male presents complaining of extreme weakness, 20-lb weight loss, lightheadedness, and dizziness. On physical exam, he appears ill, and his blood pressure is 90/70 mm Hg. He has dark skin and hyperpigmented creases on his palms. Serum sodium is low, potassium is elevated; urea level and serum calcium are both elevated as well.
A
Addisons dz (adrenal insufficiency)
8
Q
What causes addisons disease
A
autoimmune factors (70% of cases), infections, or disease within the adrenal gland. This causes a decrease in cortisol secretion and increased ACTH
ADDison’s disease = ADrenal Down or “ADD” hormone to treat ADDison’s
9
Q
What are the electrolyte findings of primary adrenal insufficiency
A
HYPERkalemia and HYPOnatremia
10
Q
What are the secondary causes of adrenal insufficiency?
A
Deficient secretion of ACTH by the pituitary gland which may be isolated or occur in conjunction with other pituitary hormone deficiencies. ACTH and cortisol levels both are low.
- Secondary factors include a pituitary adenoma or discontinuation of steroid use
11
Q
Primary or secondary
PITUITARY FAILURE which results in ↓ Cortisol, ↓ ACTH (from pituitary failure), and normal aldosterone with little or no ACTH response with the administration of CRH
A
Secondary adrenocortical insufficiency
12
Q
Initial dx for chronic adrenal insufficiency
A
8 AM serum cortisol + plasma ACTH along with an ACTH stimulation test (should be high dose)
- Elevated ACTH with low cortisol is diagnostic of primary adrenal insufficiency, particularly in patients who are severely stressed or in shock
- Low ACTH and low cortisol suggest secondary or tertiary adrenal insufficiency
13
Q
What are common lab findings associated with adrenocortical insufficiency
A
- WBC count with moderate neutropenia, lymphocytosis, and total eosinophil count over 300/μL
- Low serum Na+ (aldosterone causes sodium reabsorption and potassium excretion => low aldosterone = sodium excretion and potassium reabsorption)
- Elevated K+ (aldosterone causes sodium reabsorption and potassium excretion => low aldosterone = sodium excretion and potassium reabsorption)
- Low fasting blood glucose (due to lack of cortisol => cortisol stimulates gluconeogenesis)
14
Q
What is expected of cortisol levels after giving cosyntropin in a pt with suspected adrenocortical insufficiency
A
- Cortisol levels are low or fail to rise after giving cosyntropin (ACTH1-24) stimulation test (confirmatory)
15
Q
Addisons aka primary adrenal insufficiency tx
A
Steroids + mineralcorticoids
Hydrocortisone or Prednisone + fludrocortison (mineral)
16
Q
Tx for adrenal crisis
A
Emergent IV saline, glucose, steroids
17
Q
Cushing syndrome is caused by
A
Cushy = too much cortisol→ d/t ACTH excess → Pituitary adenoma
High cortisol, low K+, high BP
18
Q
Why does cushing disease cause a decrease in potassium?
A
Cortisol, at high levels, acts like a mineralocorticoid (aldosterone), stimulating the absorption of sodium and excretion of potassium at the collecting tubules. Hence, any disorder involving an excess of mineralocorticoids will cause hypokalemia
19
Q
Sx of cushings
A
- Fat redistribution (buffalo hump, moon facies), pigmented striae, obesity, skin atrophy, weight gain, easy bruising, elevated glucose, infections, cataracts, and hirsutism
20
Q
Why do people gain weight with Cushings?
A
Cortisol stimulates fat and carbohydrate metabolism for fast energy and stimulates insulin release and maintenance of blood sugar levels. The end result of these actions can be an increase in appetite”
21
Q
Dx of cushings
A
- Gold standard test → Twenty-four-hour urine test: A test in which urine is collected for 24 hours to measure the amounts of cortisol. A higher than normal amount in the urine may be a sign of disease in the adrenal cortex
- Dexamethasone suppression test
22
Q
Tx of cushings
A
Cushing’s disease (pituitary/secondary) is treated with transsphenoidal surgery
- Cushing syndrome (primary) ectopic or adrenal tumors: the tumor is removed - ketoconazole is given in inoperable patients
- Iatrogenic steroid therapy - begin gradual steroid withdrawal to prevent Addisonian crisis
23
Q
5-year-old male complaining of an unabated thirst that began three weeks ago. He is constantly drinking and goes to the bathroom around five times a night. He has lost five pounds over the last few weeks. The patient is on lithium for bipolar disorder. His BP is 115/70. The patient’s labs are significant for serum Na of 145 mEq/L (normal: 135-145). Urine osmolality is 185 mOsm/kg, and urine specific gravity is 1.004 (normal: 1.012 to 1.030).
A
Diabetes insipidus
24
Q
What causes diabetes insipidus
A
deficiency of or resistance to vasopressin (ADH), which decreases the kidneys’ ability to reabsorb water, resulting in massive polyuria
25
2 types of diabetes insipidus
**Central** → no _ADH PRODUCTION_
**Nephrogenic** → ADH produced, but _kidney doesnt RECOGNIZE it_
26
MCC for central diabetes insipidus
* **No ADH production most common type:** idiopathic, **autoimmune destruction of posterior pituitary** from head trauma, brain tumor, infection, or sarcoidosis
27
MCC for nephrogenic diabetes insipidus
* **Partial or complete insensitivity to ADH**: caused by drugs (Lithium, Amphoterrible), hypercalcemia and hypokalemia affect the kidney's ability to concentrate urine, acute tubular necrosis
28
Dx of diabetes inspidius
**Serum osmolality (concentration) is high** (unable to stop the secretion of water into the kidneys so blood becomes more concentrated) and **urine osmolality is low** because it is so dilute
* **Water deprivation test** – simplest/most reliable method - continued production of dilute urine despite water deprivation
* **Desmopressin stimulation test:**
* Central: reduction in urine output indicating a response to ADH
* Nephrogenic: continued production of dilute urine (no response to ADH) because kidneys can’t respond
29
Tx of diabetes inspidius
* Central = desmopressin/DDAVP
* Nephrogenic = sodium and protein restriction, HCTZ, indomethacin
30
11-y/o girl brought to you by her mother who reports **weight loss** along with **increased thirst** and **urination.** The patient has felt tired and nauseous. On examination her weight is below the 5th percentile, she looks thin, and her skin is pale. her blood pressure is 100/70 and her pulse is 104 bpm. **Her respirations are deep at a rate of 28 breaths/minute. Her breath smells fruity.**
DM type I
31
Etiology of DM type I
Autoimmune- HLA-DR3/4/O antibodies. Islet cell antibodies
32
Sx of DM I
* Polyuria, polydipsia, polyphagia, fatigue, and weight loss
* Often first recognized as diabetic ketoacidosis:
* Symptoms: Fruity breath, nausea, vomiting, dehydration
33
Tx of DM type I
Insulin
34
What is the Dawn phenomenon
Normal glucose until 2-8 am when it rises. Results from decreased insulin sensitivity and a nightly surge of counter-regulatory hormones during nighttime fasting
* Treat with bedtime injection of NPH to blunt morning hyperglycemia, avoiding carbohydrate snack late at night
35
What is the somogyi effect
Nocturnal hypoglycemia followed by rebound hyperglycemia due to a surge in growth hormone
* Treat with decreased nighttime NPH dose or give bedtime snack
36
DKA tx
* **Diabetic ketoacidosis (DKA)** should always be handled in a hospitalized setting, usually an intensive care unit, and often with an endocrinologist’s consultation, if appropriate.
* TREAT WITH FLUIDS! Patients with DKA are always dehydrated and need large-volume IV fluid resuscitation, usually isotonic fluids such as normal saline. If the corrected serum sodium level is high, this can be reduced to half-normal saline. Insulin should always be administered by an IV pump to guard against accidental overdose.
37
Dx of DM
* **Random blood glucose** level of **\> 200 mg/dL + diabetic symptoms**
* **2 separate fasting** (8 hours) glucose levels of **\> 126 mg/dL**
* **2-hour plasma glucose of \> 200** on an oral glucose tolerance test (3-hour GTT is the gold standard in GDM)
* Hemoglobin **A1c of \> 6.5%**
38
How often should A1c be checked
Hemoglobin A1c
* Represents **mean glucose level** from the **previous 8-12 weeks** (approx lifespan of an RBC)
* Useful to gauge the "big-picture" overall efficacy of glucose control in patients (either Type 1 or Type 2) to assess the need for changes in medication/insulin levels
39
What is the tx goal of A1c
* **Treatment goal of A1c \< 7.0%**
40
Tx goal of DM with finger stick glucose monitoring
* seful for insulin-dependent (either type 1 or 2) diabetics to monitor their glucose control and adjust insulin doses according to variations in diet or activity
* Treatment goals: **\< 130 mg/dL fasting** and **\< 180 mg/dL peak postprandial**
41
Dx of DM type II
**random glucose \> 200 x two**
**fasting glucose \> 126 x two**
**A1c of \> 6.5%**
42
MC Tx of DM
MC = Metformin **decreases hepatic glucose production** and peripheral glucose utilization, decreases intestinal glucose absorption (these are reasons it leads to weight loss)
* Side effects: Lactic acidosis, GI side effects, **initiation** is **contraindicated** with **eGFR \<30 mL/min** and not recommended with **eGFR 30 to 45 mL/min**, discontinue **24 hours before contrast** and **resume 48 hours after** with monitoring for creatinine, **stop if creatinine is \> 1.5**
43
Dx criteria for prediabetes
* A1C **5.7 - 6.4**
* **Fasting glucose 100 - 125**
* **2-hour** oral glucose tolerance test **140-199**
44
What are the glucose goals and mgmt of DM
* **A1C \< 7.0 %** check **every 3 months if not controlled** and **2x per year if controlled**
* **Preprandial** glucose **80-130 mg/dL** (60-90 if pregnant)
* **Peak postprandial** (1 to 2 hours after beginning of the meal) blood glucose **\< 180 mg/dL**
* Annual dilated eye exams, ACEI if microalbuminuria, annual foot examination
* **Blood pressure**
* **ACC/AHA blood pressure targets** - the target for patients with comorbidities is **\< 130/80**
* **JNC 8 treatment targets:** Reduce BP to **\< 140/90** mm Hg for everyone \< 60 including those with a kidney disorder or diabetes
45
Bone remodeling disorder that results in formation of unorganized mosaic of woven lamellar bone that is less compact and weaker than normal bone
Pagets disease of bone
46
What areas does pagets dz of bone MC affect
Pelvis, skull, spine, and legs
47
RF of pagets dz of bone
Family history
48
Sx of Pagets dz of bone
Symptomless for long periods of time; When symptoms occur its bone deformities, broken bones, pain in affected area
49
Dx of Pagets dz of the bone
Xray → Lytic lesions and thickened bone cortices; Bone bx may be done to r/o malig
50
What are common lab findings in pagets dz of bone
Increase alk phose and osteoclastic and osteoblastic activity
51
Tx of Pagets dz of bone
Bisphosphonates and calcitonin; Surgery may correct bone deformities, decompress impinged nerves, reduce fractures
52
Catecholamine secreting adrenal tumor
Pheochromocytoma
53
Sx of pheochromocytomas
Associated with neurfibromatosis type 1 and Von Hippel-lindau dz
**5 Ps** → pressure, pain (HA), perspiration, palpitations, palllor
54
Dx of pheochromocytoma
24hr catecholamines including metabolites
MRI or CT of abd to visualize tumor
55
Tx of pheochromocytoma
**Tx w/ complete adrenalectomy**; Preop tx with nonselective a blockade (phenoxybenzamine or phentolamine followed by bblockers to control HTN
56
MC type of noncancerous tumor in the pituitary gland
Pituitary microadenomas ; less than 1cm in diameter
Macroadenomas are larger than 10mm
57
Sx of pituitary adenoma
Diminished temporal vision, or bitemporal hemianopsia
58
Prolactinoma sx
Amenorrhea, galactorrhea, HA;
Location of mass at sella turcica → Mass presses on optic chiasm affecting visition loss
59
Corticotroph adenoma secretes
ATCH → Overproduction = Cushings syndrome
60
Study of choice to look for sellar lesions/tumors
MRi
61
Tx of pituitary tumors
Dopamine agonists → Cabergoline, bromocriptine
Ultimate tx = Transsphenoidal resection of pituitary tumor
62
MC risk of thyroid cancer
Radiation exposure; MC female 40-60
63
Sx of thyroid cancer
Hoarse voice; solitary cold nodule on thyroid uptake scan
64
Thyroid cancer MC type
Papillary carcinoma
65
Dx of thyroid cancer
US → All lesions\>1cm should be biopsied
Smaller lesions can be reevaluated if continues to gro
66
High risk of malignancy for thyroid cancer found on US
Microcalcifications, solid cold nodule, irregular nodule margins, nodule that is taller than it is wide
67
To evaluate thyroid malignany, what dx study is done
Thyroid uptake scan; Cancerous does not take up iodine (cold nodule)
Noncancerous will take up iodine (hot nodule)
68
If a cold nodule is found what add'l workup is needed
Fine needle aspiration
69
Tx of thyroid cancer
Depends on staging (99% 5-yr survival with local confined, 1cm papillary carcinoma)
70
Hemifacial weakness/paralysis of muscles innervated by CN VII d//t swelling of cranial nerve
Bells palsy
71
MCC of Bells palsy
Unknown; Viral etiology (herpes simplex) and ischemic factors implicated
72
How does a pt present differently in Bells palsy than in a stroke
Stroke pts are able to wrinkle forehead
Bells palsy they can not → facial weakness/paralysis wont allow it
73
What type of dx could be considered in a pt with Bells Palsy
EMG testing of nerve if paresis fails to resolve within 10 days
74
Weak bulging spot on the wall of brain artery; Usually genetic predisposition
Cerebral aneurysm
75
Sx of cerebral aneurysm
Usually asymptomatic unless ruptured; When ruptured → Sudden, severe HA
76
MC type of cerebral aneurysm
Saccular (Berry) aneurysm
77
RF of cerebral aneurysm
Smoking, htn, hypercholest, heavy alcohol; Polycystic kidney and coarctation of aorta
78
Sx of cerebral aneurysm
Sudden onset unusually severe worst headache of your life; N/V, seizure, AMS, increased BP, fever 102
79
Dx of cerebral aneurysm
Found incidentally in pts presenting with subarachnoid hemorrhage
**NONCONTRAST CT**
80
Tx of cerebral aneurysm
Surgical clipping
81
Two main types of cerebral vascular accident (CVA)
Ischemic stroke → Caused by blockage
Hemorrhagic stroke → Rupture of blood vessel
82
Sx of cerebral vascular accident
Acute onset of focal neurologic deficits resulting from either ischemia or hemorrhagic
Contralateral paralysis: Right sided symptoms d/t left sided stroke; Left sided from right sided stroke
Carotid/Opthalmic = Amarouis fugax
MCA - Aphasia, neglect, hemiparesis
ACA - Leg paresis, hemiplegia, urinary incontienenec
83
Dx of CVA
CT WITHOUT CONTRAST
84
Tx of CVA
IV tPA withing 3-4.5hrs of symptom onset
Endarterectomy if carotid \>70% occluded
85
Unilateral excruciating sharp, searing, or piercing pain often at night, lacrimation, and nasal congestion
Cluster HA
86
Tx of cluster HA
100% oxygen at 6-12L/min for 15 min via nonrebreather mask
87
GCS for eye opening
1-4
1 → None
2→ To pain
3→ To voice
4 → Spontaneous
88
GCS for verbal respomse
1-5
1→ None
2→ No words, only sounds
3→ words, but not coherent
4 → Disoriented conversation
5 → Normal conversation
89
GCS for motor response
1-6
1 → None
2 → Decerebrate
3 → Decorticate posture
4 → Withdraws to pain
5 → localizes to pain
6 → Normal
90
What GCS is classified as a coma
\<9 = Coma
91
Idiopathic pain syndrome disproportionate to injury
Complex regional pain syndrome
92
Sx of complex regional pain syndrome
Non-dermatomal limb pain; Folllowing injury, trauma
93
Dx of complex regional pain syndrome
Budapest consensus criteria
94
Tx of complex regional pain syndrome
Neurontin, elavil, bisphosphonates
95
Concussion or mild traumatic brain injury GCS score
13-15 GCS; Consciousness loss \<30 min
96
How is delirium differentiated from dementia
Delirium → Acute REVERSIBLE syndrome caused by medical condition
Dementia → Neurocognitive disorder with long-term impaired memory disease, IRREVERSIBLE such as Alzheimers dz
97
Bet-amyloid plaques + neurofibrilly tangles
Associated with Alzheimer
98
Tx of Alzheimer
Anticholinesterase drugs (Tacrine, Donpezil)
99
What are common sx of frontotemporal lobar degeneration
**Personality changes,** language difficulties, behavioral disturbances
100
Lewy Body Disease is associated with
Parkinsonian symptoms; hallucinations and delusions; Gait difficulties and falls
101
Acute inflammation of the brain; Infection may be bacterial or viral
Encephalitis
102
Etiology of encephalitits
Usually viral; MC = HSV; Immunocompromised = CMV
103
Sx of encephalitis
Fever, HA, AMS, seizures, personality changes
104
Differentiated meningitis from encephalits
Encephalitis → Altered mental status, seizures, personality changes
105
Dx of Encephalitis
Lumbar puncutre and MRI; PCR for viruses
106
Tx of encephalitis
Treat supportively; Acyclovir until HSV and Zoster are r/o
107
First line tx for essential tremor
Bblocker → Propanolol reduces limb tremors
108
Guillan-Barre sx
Ascending paralysis beginning in distal limbs; leg weakness → Total paralysis of all 4 limbs, facial muscles, eyes, loss of reflexes
109
When does Guillan Barre often present
After vaccination; **Post infectious cause = campylobacter jejuni (MC)**
CMV, Epstein barr, HIV
110
Dx of Guillan Barre
Lumbar puncture → Elevated CSF protein w/ normal CSF WBC
111
Tx of Guillan Barre
Plasma exchange (remove circulating antibodies) and IVIG
112
Most glial tumors are malignant, what are the 3 main types
Astrocytoma
Ependymoma
Medulloblastoma → MC primary malignant in children
113
Dx of intracranial tumors
Head CT or MRI with contrast
Arteriography → Stretching or displacement of cerebral vessles
EEG → Focal disturbances resulting from neoplasms
114
Classic triad of meningitis
HA, fever, stiff neck (nuchal rigidity)
115
MCC of meningitis
Viral infection
116
Difference in encephalitis and meningitis
No mental status changes in Meningitis
117
MCC of meningitis + rash
N. meningitidis → Petechiae
118
PE findings associated with meningitis
Kernig sign + Brudzinski sign
119
MC bugs in meningitis
S. pneumoniae, N. Meningiditis
Immunocompromised = Cyptococcccus
120
Viral etiology of meningitis
Most cases in US = Enterovirus
Other virsuses = Herpes, HIV, mumps, west nile
121
Fungal etiology in meningitis
Cryptococcal in immunesupressed
122
Dx of meningitis
Spinal tap, evaluating CSF
123
Bacterial vs viral CSF findings in meningitis
Bacterial - Increase protein and decreased glucose (protein love to eat glucose)
Viral - No specifics, increase lymphocytes
124
Tx of meningitis
Dexamethasone + empiric IV abx (cephalosporins, vanco, PCN)
125
If household members have been in contact with meningitis pts what is the tx
Rifampin, Cipro, Levaquin, azithro, ceftriaxone
126
Immune system disease that eats away at protective covering of nerves (myelin)
Multiple sclerosis
127
Sx of MS
Visual disturbances over many years; sensory loss, optic neuritis, weakness, paraesthesias
128
Lhermittes sign in MS
Electrical shock sensation in limbs/torso brought on by flexion of the neck
129
MC of MS
Relapsing/remitting - symptoms come and go - episodic flare ups occruing over days to weeks between periods of normalcy
130
Dx of MS
MRI → Looking for plaques (Dawson fingers aka white matter lesions)
131
Dx criteria of MS
Two episodes/attacks of sx
Two different areas of the CNS involved
CSF → IgG, oligoclonal bands
132
Tx of MS
Steroids → Acute attacks
Interferon Betas Avonex → Prevent relapses
133
Autoimmune attack of acetylcholine receptors at the neuromuscular junction that results in motor problems
Myasthenia gravis
134
Sx of Myasthenia Gravis
Eye symptoms → Ptosis, diplopia
Muscle weakness → Worsens with use; Weakness in everday activities like brushing hair
135
Myasthenia gravis tx
Acetylcholine receptor antibodies
136
Simplest most diagnostic tool for myasthenia gravis
**Simplest = Tensilon test**
Acteylcholine receptor antibodies
Gold standard for diagnosis = Single-fiber electromyography (SMEG)
137
Tx of myasthenia gravis
Acetylcholinesterase inhibtors (pyridostigmine/neostigmine)
Immunesuppression → Prednisone → decreases production of autoantibodies
138
Degeneration of basal ganglia in substantia nigra leading to loss of dopamine containing neurons
Parkinsons disease
139
3 cardinal sx of Parkinsons
Rest (pill rolling) tremor
Cogwheel rigidity
Bradykinesia (slowness of movements)
140
Dx of Parkinsons
Clinical impression
Gold standard = Neurologic exam
MRI → may help in evaluating cerebrovascular dz, tumor, etc
141
Tx of Parkinsons
\<65 - Dopamine agonists → Bromocriptine, Pramipexole, Ropinirole
\>65 Sinemet aka Levodopa/Carbidopa (S/e → GI upset, N/V vivid dreams, nightmares, psychosis, diskinesias)
142
Peripheral neuropathy sx
Symmetrical, stocking and glove distribution ; Postural hypotension
143
Tx of peripheral neuropathies
Gabapentin; TCA → Amitriptyline; Topiramate, tramadol, NSAIDS
Complications → Charcots joints
144
Status epilepticus sx
Single epileptic seizure lasting more than 5 minutes or 2 or more seizures within a 5 minute period without returning normal in between them
145
Tx of status epilepticus
Benzos → Initial tx
Phenytoin is given after benzos
146
Transient episode of neurlogic dysfunction d/t focal brain, retinal or spinal cord ischemia WITHOUT acute infarction
Transient ischemic attack (TIA)
147
Sx of internal carotid artery TIA
Amaurosis Fugax → Monocular vision loss aka lampshage down on one eye; weakness in contralateral hand
148
Dx of TIA
CT wihout contrast
Carotid Dopple US to look for stenosis
149
Tx of TIA
Aspirin or Clopidogrel aka Antiplts within 24hrs
Hospital admission for new onset and recurrent
150
**Hyponatremia /** [**Hypervolemia**](https://smartypance.com/lessons/fluid-electrolyte-disorders/hypervolemia/)
* *High risk is **ETOH**, malnourished*
* **Hypervolemic hyponatremia –** CHF, nephrotic syndrome, renal failure, cirrhosis
* **Euvolemic hyponatremia** – [SIADH](https://www.picmonic.com/palife/2586), steroids, hypothyroid
* **Hypovolemic hyponatremia** – sodium loss (renal, non-renal)
151
Hyponatremia Sx
* Acute can cause coma, brainstem herniation, **seizures**
* death not seen in chronic hyponatremia
* **chronic hyponatremia can** have motor and gate **problems which** makes them at increased **risk of falls**
* Correcting chronic low sodium can lead to osmotic demyelination syndrome
* simultaneous low K+, sodium\<105
152
Causes for hypernatremia
Definition: serum **sodium of \> 145 mmol/L**
## Footnote
Etiology: Diarrhea, burns, diuretics, hyperglycemia, diabetes insipidus, a deficit of thirst
153
Hypernatremia sx
Poor skin turgor, dry mucous membranes, flat neck veins, hypotension, **increased BUN/CR ratio \> 20:1**
154
Hyperkalemia causes
* **Seen in the late stages of** [**kidney failure stage 5**](https://smartypance.com/lessons/end-stage-renal-disease-esrd/)
* Can be seen in spironolactone and ACEI use and [acute renal failure](https://smartypance.com/lessons/acute-renal-failure-reeldx174/)
Presentation: **Peaked T waves** prolonged QRS, muscle fatigue
155
Hypokalemia causes
* Overuse of diuretics
* Cushing’s syndrome
156
Sx of hypokalemia
Presentation: Muscle cramps, constipation, **flattened/inverted T waves, U waves**
157
MCC of hypocalcemia
Hypoparathyroid
158
Causes of hypocalcemia
* The most common cause is [hypoparathyroidism](https://smartypance.com/lessons/parathyroid-disorders-pearls/hypoparathyroidism/)
* Other causes
* Thyroid surgery (injuring the parathyroid gland)
* Renal disease
159
ECG findings of Hypocalcemia
Presentation: QT prolongation, [Trousseau’s sign](https://youtu.be/Ry5Rh3wO8Sw), [Chvostek’s sign](https://youtu.be/2tV4J2DxjNM)
* Labs: **↓ Ca+ ↓ PTH ↑ phosphate**
* **EKG = Prolonged QT**
160
MCC of Hypercalcemia
* [Sarcoidosis](https://smartypance.com/lessons/restrictive-pulmonary-disease/sarcoidosis/)
* [Tuberculosis](https://smartypance.com/lessons/mycobacterial-disease/tuberculosis-reeldx471/)
* [Paget disease](https://smartypance.com/lessons/metabolic-disorders-pearls/paget-disease/)
* **Metastatic cancers to bone (**[**prostate**](https://smartypance.com/lessons/neoplastic-diseases-genitourinary-system/prostate-cancer/)**,** [**breast**](https://smartypance.com/lessons/neoplasms-of-the-breast-and-reproductive-tract/cancer/)**,** [**ovarian**](https://smartypance.com/lessons/neoplasms-of-the-breast-and-reproductive-tract/neoplasms/)**,** [**renal**](https://smartypance.com/lessons/neoplastic-diseases-of-the-renal-system-pearls/renal-cell-carcinoma/)**)**
* [**Multiple myeloma**](https://smartypance.com/lessons/hematologic-malignancies/multiple-myeloma/)
161
Hypercalcemia sx
Presentation: **“Stones, bones, abdominal groans, psychiatric moans”, EKG: shortened QT interval.**
162
Hyperphosphatemia causes
Definition: serum **phosphate \> 4.5 mg/dL**
Etiology: [Chronic kidney disease](https://smartypance.com/lessons/renal-diseases/chronic-kidney-disease/)
163
Insulin secretagogues (aka sulfonylureas and meglitinides) - MOA and ADEs
Increase insulin secretion by inhibiting b-cell K-ATP channels
**ADE: Hypoglycemia + Weight gain**
164
Biguanides aka Metformin - MOA + ADE
MOA = Stimulate AMPK and inhibit mitochondrial gluconeogenesis + **Decreasing hepatic glucose production + increasing peripheral glucose uptake**
ADE= Diarrhea + lactic acidosis
165
TZDs (Pioglitazone) MOA + ADE
Activate transcription regulator PPAR-y → Decrease insulin resistance
ADE= Fluid retention/heart failure + weight gain **aka EDEMA + Weight gain**
166
GLP-1 Agonists (exenatide + liraglutide) MOA + ADE
Increase glucose dependent insulin secretion, decrease glucagon secretion, delayed gastric emptying
ADE = **Pancreatitis + weight loss**
167
DPP4 Inhibitors (Sitagliptin + Saxagliptlin) MOA + ADE
MOA = Increase endogenous GLP-1 & GIP levels
ADE= **Nasopharyngitis**
168
SLGT2 Inhibitors (Canagliflozin +Dapagliflozin) MOA + ADE
MOA = Increase renal glucose excretion
## Footnote
**ADE= UTI (increase in peeing sugar = increase in candida) + Hypotension**
