Iqra Asghar @iqrajaffri14 on GrepMed

Quincke's Pulse in Severe Aortic Regurgitation Little physical exam finding for the end of the week! Quinke’s Pulse in chronic severe AI! Many of the physical exam findings relate to the high stroke volume, widened pulse pressure, and rapid arterial pressure drop associated with chronic AI! Dr. Jay Mohan, D.O. RPVI @DrJayMohan #Quinckes #Quinkes #Pulse #AorticRegurgitation #Diagnosis #PhysicalExam #Fingernails #Nailbed #Cardiology

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Primary and Secondary Causes of Hypertension - Differential Diagnosis Algorithm Primary (Essential) (95%) - Onset between age 20 and 50. Positive family history. No features of secondary hypertension. • Long-standing • Uncontrolled • Drug Withdrawal Mislabelled - Repeatedly normal blood pressure when taken at home, work or when using an ambulatory monitor. • White-coat Hypertension • Masked Hypertension Secondary Causes (5%) - Onset age < 20 or > 50 years, No family history. Hypertensive urgency. Resistant hypertension. - Exogenous • Corticosteroids • Oral Contraceptive Pills • Cocaine • Black licorice • Medications - Renal • Renal parenchymal disease - CKD, AKI, Glomerulonephritis • Renovascular disease (unilateral and bilateral renal artery stenosis) - Mechanical • Aortic coarctation • Obstructive Sleep Apnea - Endocrine • Glucocorticoid excess (Cushing syndrome or disease) • Catecholamine excess (pheochromocytoma) • Mineralocorticoid excess (primary aldosteronism) • Hyperthyroidism (mainly systolic hypertension) • Hypothyroidism (mainly diastolic hypertension) • Hyperparathyroidism • Pregnancy (Gestational hypertension) #Hypertension #Primary #Secondary #HTN #Cardiology #Differential #Diagnosis #Algorithm #causes

Photophobia and Headache - Differential Diagnosis Framework Why? • The coexistence of photophobia and headache suggests the potential reciprocal interactions between visual and pain pathways. • Interactions between visual and pain pathways occur at the retina, midbrain, thalamus, hypothalamus, and visual cortex. • In migraines: photophobia could result from photic activation of retina-driven pathways involved in the regulation of homeostasis. Primary headaches: • Migraine: - 80 percent of people who have migraines have photophobia - Bilateral photophobia - Severe persistent photophobia - Migraine with aura > migraine without aura - Chronic migraine > episodic migraine - Benign episodic mydriasis, miosis • Tension-type headache: - Bilateral or unilateral photophobia - Mild persistent photophobia • Trigeminal autonomic cephalalgias (TACs): - Hemicrania continua, SUNCT, SUNA, etc. - Unilateral - Reversible, only during their cluster period - Moderate, between migraine and tension-type headache - Autonomic symptoms - Miosis Secondary headaches: • Traumatic brain injury (TBI): - Reversible or persistent photophobia • Meningitis: - Patients tend to have meningeal irritation signs - Photophobia in viral meningitis is the most common form • Non-traumatic subarachnoid hemorrhage (SAH): - Mydriasis - Can have isolated photophobia without headache • Disorder of the eyes - Photophobia often precedes the onset of headache: - Acute angle-closure glaucoma - Ocular inflammatory disorder - Trochlear headache • CNS Vasculitis Painful cranial neuropathies: • Trigeminal neuralgia: - Common in patients with the first division of the trigeminal nerve pain - Mydriasis • Painful optic neuritis #Photophobia #Headache #differential #diagnosis #ophthalmology #Neurology

SNOOP mnemonic may catch potentially life-threatening headaches Systemic signs and disorders Neurologic symptoms Onset new or changed & patient >50 years old Onset in thunderclap presentation Papilledema, Pulsatile tinnitus, Positional provocation, Precipitated by exercise #SNOOP #mnemonic #headaches #Differential #Diagnosis #headache #redflag #dangerous #neurology

There are similarities and differences between these 3 conditions which all carry treatment implications. Each mimic the “Starved state” where Glucagon easily outweighs Insulin. Glucagon stimulates the breakdown of glycogen stores in the liver along with Gluconeogenesis to maintain blood glucose. It also stimulates Lipolysis, which mobilizes fatty acids for beta-oxidation in the liver to produce Acetoacetic acid, a ketoacid that is also converted to beta hydroxybutyrate (BHB). Therefore, in all 3 conditions, serum BHB has limited utility in differentiation. In Starvation Ketosis (SK), acidosis is very mild if at all present. Ketoacids stimulate the pancreas to release Insulin which is enough to keep Lipolysis in check. In Alcoholic Ketoacidosis (AK) we commonly encounter patients who are severely volume depleted and in withdrawal which drastically elevates the stress level along with circulating stress hormones that work synergistically with Glucagon to overwhelm Insulin. This leads to massive production of Ketoacids like BHB. But we also have Lactic Acidosis as well. Recall, NAD+ is a cofactor used to convert Pyruvate to Acetyl-CoA in the TCA cycle. The metabolism of Alcohol depletes NAD+ yielding NADH instead, a cofactor used to convert Pyruvate to Lactate! Patients with AK may, therefore, present with severe acidosis. NAD+ is also a cofactor for Gluconeogenesis which is why patients may also present with Hypoglycemia. In both SK and AK, feed them or give IV dextrose, give thiamine, and watch out for Refeeding Syndrome. If Hyperglycemic, avoid Insulin drips unless also diabetic as you risk causing Hypoglycemia once the Insulin/Glucagon balance normalizes. In both conditions, low levels of circulating Insulin and Ketoacid-induced Insulin release are typically enough to prevent blood glucose > 250 mg/dl or Glucosuria. DKA is essentially a state of NO Insulin; the actions of Glucagon are completely unmitigated, and this leads to severe ketoacidosis, Hyperglycemia > 250 mg/dl and Glucosuria. Treat with Insulin, provided the starting potassium is appropriate to do so. #diagnosis #differential #algorithm #management #treatment #criticalcare #foamed