Endocrine and Electrolytes Flashcards
Early signs of Fe++ Toxicity
Vomiting and Bloody Diarrhea
Can progress to bloody vomit
Convulsions & Tetany are signs of
HypOcalcemia
Ataxia + Colicky Abdominal Pain are signs of
Early Pb Poisoning
Purple Striae + a supraclaviular or posterior cervical fat pad are signs of:
Cushing’s Disease
Posterior Fat Pad is known as a buffalo hump
TOO MUCH CORTISOL!!!
Name an element that, with chronic use, can induce Diabetes Insipitus
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.
Pituitary Dwarfism vs Achondroplasia
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
Pretibial Myxedema
What is it?
Sign of?
Red Peau d’Orange swollen plaques on the anterior aspect of the tibia
Seen in Hyperthyroidism, called Graves Dermatitis
Normal BUN, Cr, Cr Cl, GFR
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
Uremic
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
Find a solitary Thyroid Nodule on physical Exam, TSH normal, next step:
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.
Hot vs Cold Thyroid Nodules
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.
Brown pigmentation, fatigue, weakness, loss of appetite, weight loss and syncope. Think
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
Pheochromocytoma
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
Gradual Onset Bitemporal Hemianopsia, think
Something is pressing on the optic chasm
Pituitary tumor.
Get an MRI
Sulfonureas and Meglitinides…
“Ides + Glinides”
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
Thiazolidinediones
“Glitazones”
ACTOS + AVANDIA
PPAR Activators
These are no no-s.
Actos/PioGlitazone Bladder Cancer
Avandia/ RosiGlitazone Heart Failure/Death
GLP-1 Agonists
“Tides + GluTides”
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…
DPP4 Inhibitors
The “Gliptins”
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
SGLT-2 Inhibitors
“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?
