Endocrine and Electrolytes

Question 1

Early signs of Fe++ Toxicity

Answer 1

Vomiting and Bloody Diarrhea

Can progress to bloody vomit

Question 2

Convulsions & Tetany are signs of

Answer 2

HypOcalcemia

Question 3

Ataxia + Colicky Abdominal Pain are signs of

Answer 3

Early Pb Poisoning

Question 4

Purple Striae + a supraclaviular or posterior cervical fat pad are signs of:

Answer 4

Cushing’s Disease

Posterior Fat Pad is known as a buffalo hump

TOO MUCH CORTISOL!!!

Question 5

Name an element that, with chronic use, can induce Diabetes Insipitus

Answer 5

Lithium…

Watch your Bipolar Patients for excessive thirst and urination

Li somehow interacts with the Na/K pump preventing Na+ movement BACK into the cell which makes the ECF salty which makes you thirsty which makes you pee which flushes all your sodium and you end up hyponatremic.

Question 6

Pituitary Dwarfism vs Achondroplasia

Answer 6

Achondroplasia (Disproportionate Dwarfism) is the most common form of dwarfism characterized by disproportionately short limbs and digits. It is usually apparent at birth. Normal Intellectual capacity. Caused by genetically impaired chondrocytes.

Pituitary Dwarfism (aka Proportionate Dwarfism) is a growth hormone deficiency resulting in overall small stature, below the 3rd percentile on growth charts as the child grows (or doesn't)
Because growth hormone does other things in the body than cause growth, this deficiency may cause issues in multiple organ systems and needs to be rectified at least to

Question 7

Pretibial Myxedema

What is it?

Sign of?

Answer 7

Red Peau d’Orange swollen plaques on the anterior aspect of the tibia

Seen in Hyperthyroidism, called Graves Dermatitis

Question 8

Normal BUN, Cr, Cr Cl, GFR

Answer 8

BUN 6-20

Cr 0.6-1.2 female (wider for male: 0.5-1.5)

Cr Cl normal +/- 140 v.close to GFR

GFR norm is over 90, healthy 140

Question 9

Uremic

Answer 9

Pt in acute renal failure, BUN + Cr are way out of range and Uric Acid is backing up into the blood

Sxs:  Itching (Pruritis)
         Dry skin (Xerosis)

Signs: HypERtension
there’s so much stuff in the
blood its drawing fluid in to
dilute it

Common in uncontrolled DM

Question 10

Find a solitary Thyroid Nodule on physical Exam, TSH normal, next step:

Answer 10

Need to see what’s in it
Needle Biopsy

If TSH were low, we might first do a Thyroid Scan as we’d want to know if the nodule were Hot (absorbs radioactive iodine but no risk of cancer) or COLD (doesn’t absorb the iodine and has a 5% chance of malignancy)

Most solitary thyroid nodules are cold but only 5% of them are cancerous.

Question 11

Hot vs Cold Thyroid Nodules

Answer 11

HOT: Absorbs radioactive iodine but no risk of cancer

COLD: Doesn’t absorb the iodine and has a 5% chance of malignancy

Most solitary thyroid nodules are cold but only 5% of them are cancerous.

Question 12

Brown pigmentation, fatigue, weakness, loss of appetite, weight loss and syncope. Think

Answer 12

No cortisol…

Addisons or PRIMARY Adrenal Insufficiency. Lack of/decreasing coritsol production in compromised adrenals leads to constant release if ACTH from the Anterior pituitary.

The brown is ADDISONIAN BRONZING
melanocyte stimulating hormone gets released whenever ACTH is secreted by the Anterior Pituitary.

The Low BP is due to hypovolemia. Aldosterone comes from Cortisol so no cortisol means no RAAS conservation of Na+ . Hyponatremia leads to hypovolemia leads to hypotension.

Secondary Adrenal Insufficiency would be when there is a deficiency of ACTH for some reason (In US this is usually caused by overuse of STEROIDS, could be a pituitary or hypothalamic tumor though) and thus cortisol isn’t released, though the adrenals are working fine. In this situation, there isn’t really hypovolemia as aldosterone is still being produced as is cortisol. Cortisol just isn’t being released as the pituitary can’t “call” for it.

tumors also cause OVERproduction of ACTH, in which case TOO MUCH cortisol would be released by functioning adrenals. This would be Cushings Disease

Question 13

Pheochromocytoma

Answer 13

Adrenal Tumor causes overproduction of Epi + Nor

Constant fight or flight: Anxiety, HA, Sweating, TAchy, Weight loss

Measure catacholiamines (epi, nor, dopamine) in 24 hr urine collection

Surgury to remove the tumor is the RX

Question 14

Gradual Onset Bitemporal Hemianopsia, think

Answer 14

Something is pressing on the optic chasm

Pituitary tumor.

Get an MRI

Question 15

Sulfonureas and Meglitinides…

“Ides + Glinides”

Answer 15

Block Potassium ATP channels in the Beta Cell increasing Insulin secretion

Sulphonureas- Biggest risk of hypoglycemia for oral diabetes meds, 2nd only to Insulin itself
Glipizide/Glucotrol short acting
Glimeperide/Amaryl long acting

Meglitinides - Repa + Nate These are just less
powerful than sulphonureas but work the same way.
Repaglinide/Prandin
Nateglinide/Starlix
Mitiglinide/Glufast

Question 16

Thiazolidinediones

“Glitazones”

Answer 16

ACTOS + AVANDIA

PPAR Activators

These are no no-s.

Actos/PioGlitazone Bladder Cancer
Avandia/ RosiGlitazone Heart Failure/Death

Question 17

GLP-1 Agonists

“Tides + GluTides”

Answer 17

These are commonly called the DM2 “Injectables”

GLP-1 (Glucagon Like Peptide-1), an INCRETIN that:
-Induces Beta Cell Insulin Release
-Suppresses Alpha Cell Glucagon Release
-Slows Gastric Emptying, digestion goes on long
stabilizing blood sugars over time

GLP-1 AGONISTS Mimic GLP-1 at the GLP-1 Receptor. They are able to turn it on and reap GLP-1 benefits and they:
-Don’t overshoot/oversecrete Insulin like
sulfonureas and meglitinides
-Main side effects are GI: gassy, gurgle, bloat
-Pancreatitis- but anything that messes with
the pancreas risks this

Exenatide/Byetta- Oldest, generic available
Long Acting is new, still under patent
Liraglutide/ Victoza

Lira, Dula, Abli, Exen…

Question 18

DPP4 Inhibitors

The “Gliptins”

Answer 18

Oral
DPP4 is an enzyme that inactivates GLP-1 (Glucagon Like Peptide-1), an INCRETIN that enhances Beta insulin secretion, Suppresses Alpha Glucagon secretion and slows Gastric Emptying.

DPP4- Inhibitors therefore prevent DPP4 from inactivating GLP-1, thereby allowing GLP-1 to stay in play longer.

There are DPP4 Receptors all over the airway in addition to on GLP-1. Blocking its activity at GLP-1 means blocking it in the airway + lungs as well. We don’t know exactly what this means but the main side effect of DPP4-Inhibitor use is cold symptoms and we also know that Coronaviruses also block DPP4 receptors in the airway and deliver cold/URI symptoms.

Sita      (Sita is no longer under patent)
Saxa
Lena
Vilda
Alo.....Gliptin

Question 19

SGLT-2 Inhibitors

Answer 19

“Flozins Flush!!” Farxiga + Invokanna

Glucose is 100% reabsorbed from the filtrate in the proximal tubule via SGLT-2 Transporters (Sodium, Glucose Linked Transporter).

Na/K ATP pumps on the basolateral membrane set up a Na+ gradient. Na+ flows down its gradient INTO the filtrate and Glucose is thereby allowed to flow out of the filtrate and back into the blood in the efferent arterioles of the neprhron.

Flozins block this protein transporter - gum it right the heck up, leaving all that sugar in the filtrate for deliver to the bladder and excretion.

Problems are obvious - sugar doesn’t belong in the urine and Candida LOVES sugar and candida lives in the vulva and especially on sweet diabetic people… Nasty fungal THRUSH and UTI and PYELO that are only treatable with Amphoterecin B (systemic and filling the bladder with it) and Fluconizole (systemic). Both of which are nasty courses of meds with significant side effects.

Rapid Wt Loss possible this can be good/bad
HypoGlycemia possible

Sounds great but I wouldn’t do it. Can’t even imagine how to take it such that the yeasts won’t go wild down there?