Fibromuscular dysplasia is characterized by abnormal tissue growth within arterial walls, resulting in stenotic and tortuous arteries that can cause tissue ischemia and are prone to aneurysm formation. Pathology typically demonstrates alternating fibromuscular webs and aneurysmal dilation with absent internal elastic lamina (string-of-beads appearance). Renovascular hypertension occurs due to renal artery stenosis and activation of the renin-angiotensin-aldosterone system. make small HY note with IMP stuff NBME test maker lever sticky note

Generating Image

Here is your HY sticky note on FMD:

📌 FIBROMUSCULAR DYSPLASIA (FMD) - HY Sticky Note

WHO: Young/middle-aged women (F >> M) | No atherosclerosis risk factors

ARTERIES HIT (in order):

Renal (most common) → Carotid/Vertebral → Mesenteric

BUZZWORD PATHOLOGY:

Alternating stenosis + aneurysmal dilation = "String of beads" on angiography
Absent internal elastic lamina
Most common type = medial fibroplasia
NO intimal plaques, NO calcification (distinguishes from atherosclerosis)

CLASSIC PRESENTATION:

Young woman + renovascular HTN + flank/abdominal bruit → Renal artery stenosis → RAAS activation → ↑ Renin → ↑ Angiotensin II → HTN

COMPLICATIONS:

Renovascular HTN
Arterial dissection (spontaneous)
Aneurysm rupture
Tissue ischemia (bowel, brain, kidney)

DX: CT angiography or catheter angiography TX: Percutaneous transluminal angioplasty (PTA) - first line; NO stent needed typically

DIFFERENTIALS - Don't Mix Up:

Feature	FMD	Atherosclerosis	Takayasu
Age/Sex	Young women	Older, M = F	<40 women
Location	Mid/distal artery	Ostium/proximal	Aorta + branches
Inflammation	No	No	Yes (granulomatous)
Calcification	No	Yes	No
"String of beads"	YES	No	No

NBME TRIGGER WORDS:

"Young woman with hypertension and abdominal bruit"
"String of beads on renal angiography"
"Spontaneous cervical artery dissection"
"Absent internal elastic lamina on biopsy"
"Renal artery stenosis without atherosclerosis"

KEY MECHANISM: Renal A. stenosis → ↓ perfusion pressure → ↑ Renin → Angiotensin I → ACE → Angiotensin II → vasoconstriction + aldosterone release → HTN + hypokalemia (if severe)

High-yield: FMD is the #1 cause of renovascular HTN in young women. Atherosclerosis is #1 overall.

In the location, it's best if you involve which arteries are involved, that is, the cardiovascular dysplasia, women after the carotid and vertebral arteries, and other sclerosis as you see with primary coronary artery disease, and also all perifibral disease, which can cause atherosclerosis, and then Takayasu, which artery is causing it.

Here is the updated HY sticky note with full artery location details for each condition:

📌 FIBROMUSCULAR DYSPLASIA (FMD) - HY Sticky Note

WHO: Young/middle-aged women (F >> M) | No atherosclerosis risk factors

ARTERIES HIT (FMD) - Mid/Distal segments:

Artery	Consequence
Renal (most common)	Renovascular HTN, renal ischemia
Internal carotid (extracranial)	Stroke, TIA, pulsatile tinnitus
Vertebral	Posterior circulation stroke, dissection
Mesenteric	Bowel ischemia
Celiac	Abdominal angina

Spares coronaries and aorta (distinguishes from atherosclerosis and Takayasu)

BUZZWORD PATHOLOGY:

Alternating stenosis + aneurysmal dilation = "String of beads" on angiography
Absent internal elastic lamina
Most common type = medial fibroplasia
NO intimal plaques, NO calcification

CLASSIC PRESENTATION:

Young woman + renovascular HTN + flank/abdominal bruit Renal artery stenosis → RAAS activation → ↑ Renin → ↑ Ang II → HTN

COMPLICATIONS: Renovascular HTN | Spontaneous arterial dissection | Aneurysm | Ischemia

DX: CT angiography or catheter angiography TX: Percutaneous transluminal angioplasty (PTA) - NO stent needed

ARTERY LOCATION COMPARISON TABLE

Feature	FMD	Atherosclerosis	Takayasu Arteritis
Age/Sex	Young women	Older, M = F	<40 women (Asian)
Arteries involved	Renal, carotid, vertebral, mesenteric	Coronaries, aorta, iliofemoral, carotid (proximal), renal (ostial)	Aorta + all major branches: subclavian (#1), carotid, renal, pulmonary
Segment affected	Mid/distal	Ostium/proximal	Proximal/ostial (origin from aorta)
Coronaries	Spared	YES - major target	Rare (coronary ostia)
Peripheral/limb	Rare	YES - iliofemoral → claudication, Leriche syndrome	YES - subclavian → absent radial pulse, arm claudication
Inflammation	No	No (lipid/mechanical)	Yes - granulomatous panarteritis
Calcification	No	YES	No
"String of beads"	YES	No	No
Key buzzword	Young woman + HTN + bruit	Risk factors + angina + claudication	Young Asian woman + absent pulse + ↑ ESR/CRP

PERIPHERAL ARTERY DISEASE (Atherosclerosis) - Extra HY:

Iliofemoral → Leriche syndrome: bilateral leg claudication + absent femoral pulses + erectile dysfunction
ABI < 0.9 = PAD | ABI < 0.4 = critical ischemia
Popliteal aneurysm = most common peripheral aneurysm (atherosclerotic)

NBME TRIGGER WORDS for FMD:

"Young woman + HTN + abdominal/flank bruit"
"String of beads on renal angiography"
"Spontaneous cervical artery dissection"
"Renal artery stenosis WITHOUT atherosclerosis"
"Absent internal elastic lamina"

Okay, can you make me a note like NBME level strategic approach of diabetes insipidus? without tables In that, I want what is congenital diabetes insipidus, nephrogenic diabetes insipidus, central diabetes insipidus, and what all they're gonna check. Like what are the important differentiators of diabetes insipidus and other diseases which I have to rule out in case of questions on strategic? Anything else associated with hyper or hypothyroidism and diabetes insipidus in that that book. So I think confidently you can do like a note of note of diabetes insipidus and also the hypothyroidism like primary hyperparathyroidism, secondary hyperparathyroidism, tertiary hyperparathyroidism.

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I now have all the textbook content I need. Let me compile both notes.

📌 DIABETES INSIPIDUS - NBME STRATEGIC HY NOTE

CORE CONCEPT

DI = large volume of hypotonic (dilute) urine + polyuria + polydipsia

Urine volume typically >50 mL/kg/day. Three Ps: Polyuria, Polydipsia, hypernatremia (if thirst impaired) Root problem: ADH (vasopressin/AVP) is either NOT made, NOT released, or NOT responded to

THE 5 TYPES - KNOW THEM ALL

1. CENTRAL DI (Hypothalamic/Neurogenic)

Cause: posterior pituitary/hypothalamus destroyed - can't make or release ADH
Etiology: head trauma, pituitary surgery, craniopharyngioma, sarcoidosis, histiocytosis X (Langerhans cell), TB meningitis, multiple sclerosis, idiopathic
Congenital form: autosomal dominant - usually asymptomatic in infancy, onset in childhood; defect in signal peptide or neurophysin portion of the prohormone
Key fact: need to destroy >80% of ADH-secreting neurons before symptoms appear
Vasopressin level: LOW or undetectable

2. NEPHROGENIC DI

Cause: kidney cannot RESPOND to ADH - collecting duct is resistant
Congenital:
- X-linked recessive (>90%): inactivating mutation of V2 receptor - affects males
- Autosomal recessive/dominant (<10%): loss-of-function mutations in AQP2 (aquaporin-2 water channel, chromosome 12)
Acquired causes (drugs + electrolytes):
- Lithium (most tested) - downregulates AQP2
- Demeclocycline - used therapeutically to treat SIADH
- Amphotericin B, rifampin, cisplatin, ifosfamide
- Chronic hypokalemia - downregulates AQP2
- Hypercalcemia - downregulates AQP2
- Polycystic kidney disease, sickle cell nephropathy, amyloidosis
Vasopressin level: HIGH (kidney not responding)

3. GESTATIONAL DI

Placenta makes cysteine aminopeptidase (vasopressinase) that destroys ADH
Presents during pregnancy, resolves after delivery
Vasopressin level: can't be measured (destroyed)
Responds to DDAVP (synthetic, resistant to vasopressinase)

4. OSMORECEPTOR DYSFUNCTION (Adipsic/Essential Hypernatremia)

Neurohypophysis intact, but osmoreceptor cells in anterior hypothalamus damaged
No thirst + no vasopressin release - patient does NOT have polydipsia
Classic cause: anterior communicating artery aneurysm clipping
Elevated serum Na without polydipsia = red flag

5. PRIMARY POLYDIPSIA (Psychogenic/Dipsogenic)

Excess water intake suppresses ADH - dilute urine from too much water, NOT from ADH problem
Psychogenic: schizophrenia, bipolar, OCD - prevalence up to 40% in psych hospitals
Dipsogenic: hypothalamic lesion or habit-based
Plasma osmolality: LOW-normal (opposite of true DI)
Vasopressin level: LOW (appropriately suppressed)

DIAGNOSTIC APPROACH - THE NBME ALGORITHM

Step 1 - Rule out diabetes mellitus first (glucosuria causes osmotic diuresis)

Step 2 - Check urine osmolality and plasma osmolality

Urine osm <300 mOsm/kg + plasma osm >295 = DI (not primary polydipsia)
Urine osm >300 mOsm/kg = solute diuresis (glucose, mannitol, urea)

Step 3 - Water Deprivation Test + DDAVP

Standard protocol: deprive water, check urine osm hourly until plateau, then give DDAVP

Finding after deprivation	After DDAVP	Diagnosis
Urine osm stays low (<300)	Urine osm increases >50%	Central DI
Urine osm stays low (<300)	Urine osm stays low (<10% rise)	Nephrogenic DI
Urine osm rises to near-normal	No significant rise	Primary Polydipsia

Partial Central DI: Urine osm rises but not to maximum - DDAVP causes 10-50% further rise

Step 4 - Plasma AVP (vasopressin) or Copeptin

Best modern method: hypertonic saline-stimulated plasma copeptin (cleaved from pre-pro-AVP in posterior pituitary) - can substitute for water deprivation test
Central DI: low copeptin despite high plasma osm
Nephrogenic DI: high copeptin

KEY LABS TO KNOW

Urine specific gravity: <1.005 (very dilute)
Serum Na: high-normal to frankly elevated (hypernatremia)
Serum osmolality: >295 mOsm/kg
Urine osmolality: inappropriately low relative to serum
ADH/Copeptin: low = Central; high = Nephrogenic; low (appropriately) = Primary polydipsia

TREATMENT

Type	Treatment
Central DI	DDAVP (desmopressin) - intranasal or oral; synthetic V2 agonist
Nephrogenic DI	Thiazide diuretics (paradoxical - reduce GFR/urine output) + Low Na/protein diet + NSAIDs; NOT DDAVP (won't work)
Gestational DI	DDAVP (vasopressinase-resistant)
Primary Polydipsia	Fluid restriction + treat underlying psych illness
Lithium-induced NDI	Amiloride (blocks Li entry into principal cells)

RULE-OUT DIFFERENTIALS (NBME loves these)

Diabetes Mellitus - polyuria but urine is hyperosmolar (glucosuria), serum glucose elevated
SIADH - opposite problem: too much ADH, hyponatremia, concentrated urine despite low serum osm
Psychogenic polydipsia - dilute urine from excess intake, plasma osm LOW not high
Osmotic diuresis - high urine osm (not low), look for glucose/mannitol/urea as culprit
Adipsic hypernatremia - hypernatremia WITHOUT polydipsia (no thirst)

NBME TRIGGER PHRASES FOR DI

"Head trauma patient - large urine output, high serum Na, dilute urine" = Central DI
"Male infant with polyuria, hypernatremia, no response to vasopressin" = X-linked congenital nephrogenic DI (V2 receptor mutation)
"Bipolar patient on lithium - polyuria" = Nephrogenic DI (treat with amiloride or thiazide)
"Pregnant woman with polyuria, responds to DDAVP" = Gestational DI
"Psychiatric patient - polyuria, LOW serum Na, dilute urine" = Primary polydipsia
"Hypercalcemia or hypokalemia causing polyuria" = Acquired nephrogenic DI (AQP2 downregulation)

📌 HYPERPARATHYROIDISM - PRIMARY / SECONDARY / TERTIARY

PTH ACTIONS (must know mechanism first)

PTH raises serum Ca via:

Bone - increases RANKL on osteoblasts → osteoclast activation → Ca mobilization
Kidney (tubule) - increases Ca reabsorption, increases phosphate EXCRETION (phosphaturia)
Kidney (1-alpha hydroxylase) - converts 25-OH-D → 1,25(OH)2-D (active) → gut Ca absorption

Net result: ↑ Ca, ↓ PO4

THE THREE TYPES - SIDE BY SIDE

PRIMARY HYPERPARATHYROIDISM

Cause: parathyroid adenoma (most common, solitary) > hyperplasia (multiglandular) > carcinoma (rare)
Associated: MEN1 (parathyroid + pituitary + pancreas) and MEN2A (parathyroid + medullary thyroid Ca + pheochromocytoma)
Labs: ↑ Ca, ↓ PO4, ↑ PTH (PTH inappropriately elevated for the high Ca)
Most common cause of asymptomatic hypercalcemia (found on routine blood test)
Symptoms (4 Stones, 4 Bones, 4 Groans, 4 Psychic Moans):
- Stones: nephrolithiasis (Ca-oxalate or Ca-phosphate), nephrocalcinosis
- Bones: osteoporosis, osteitis fibrosa cystica, brown tumors, dissecting osteitis ("railroad track" on X-ray)
- Groans: constipation, N/V, pancreatitis, PUD
- Psychic: depression, anxiety, cognitive changes
Normocalcemic form: normal Ca but elevated intact PTH x2 measurements - can be prelude to primary HPT
Treatment: parathyroidectomy

SECONDARY HYPERPARATHYROIDISM

Cause: physiologic response to chronic hypocalcemia - most commonly chronic kidney disease (CKD)
Mechanism in CKD: ↓ GFR → ↑ PO4 retention → ↓ Ca → ↓ 1,25-OH-D synthesis (damaged kidneys can't do 1-alpha hydroxylation) → all stimulate PTH release → parathyroid gland hyperplasia
Labs: ↓ Ca (or low-normal), ↑ PO4, ↑ PTH
PTH is elevated as a COMPENSATION - this is appropriate physiology gone into overdrive
Bone disease: milder than primary HPT (renal osteodystrophy)
Treatment: correct the underlying cause - phosphate binders, vitamin D supplementation, calcimimetics (cinacalcet)

TERTIARY HYPERPARATHYROIDISM

Cause: long-standing secondary HPT where parathyroid glands undergo autonomous (monoclonal) adenomatous change and no longer respond to feedback
Classic setting: CKD patient who gets a kidney transplant but PTH remains elevated despite normalization of Ca
Labs: ↑ Ca, ↑ PTH - now looks like primary HPT but occurs in context of prior renal failure
Mechanism: early polyclonal secondary hyperplasia evolves into monoclonal tumors - hyperphosphatemia from CKD independently drives PTH production
Treatment: parathyroidectomy

QUICK COMPARISON

	Primary	Secondary	Tertiary
Serum Ca	HIGH	Low/Normal	HIGH
Serum PO4	Low	HIGH	Variable
PTH	HIGH (autonomous)	HIGH (compensatory)	HIGH (autonomous)
Cause	Adenoma/hyperplasia	CKD (most common)	Long-standing CKD → autonomous gland
Gland change	Adenoma or hyperplasia	Hyperplasia (polyclonal)	Adenoma (monoclonal)
Key feature	Hypercalcemia on routine labs	Hypocalcemia + renal disease	Post-transplant persistent hypercalcemia

HYPERCALCEMIA CAUSES - CRITICAL RULE-OUTS

HIGH PTH causes (PTH-dependent):

Primary hyperparathyroidism (adenoma)
Tertiary hyperparathyroidism
Familial hypocalciuric hypercalcemia (FHH) - calcium-sensing receptor mutation, benign, urinary Ca is LOW

LOW PTH causes (PTH-independent):

Malignancy - most important symptomatic cause:
- PTHrP (PTH-related peptide) - squamous cell lung Ca, renal cell Ca, ovarian Ca - mimics PTH labs
- Lytic bone mets (myeloma, breast)
- Excess 1,25-OH-D (lymphoma)
Granulomatous disease: sarcoidosis, TB, histoplasmosis (activated macrophages convert 25-OH-D → 1,25-OH-D)
Vitamin D toxicity
Thyrotoxicosis
Thiazide diuretics
Milk-alkali syndrome
Vitamin A toxicity

NBME key differentiator - PTHrP vs PTH:

Both lower PO4 and raise Ca, but PTHrP is NOT detected by standard PTH immunoassay. Look for malignancy history + low PTH + high Ca.

OSTEITIS FIBROSA CYSTICA - CLASSIC HISTOLOGY

Osteoclasts tunnel along trabeculae = "dissecting osteitis" or "railroad track" appearance
Marrow replaced by fibrovascular tissue
Brown tumors = reactive fibrous tissue + hemorrhage + hemosiderin (brown color)
Cystic degeneration of brown tumors = generalized osteitis fibrosa cystica (rarely seen now - caught early)

NBME TRIGGER PHRASES

"Asymptomatic hypercalcemia on routine labs, ↑ PTH, ↓ PO4" = Primary HPT (adenoma)
"CKD patient, low Ca, high PO4, high PTH" = Secondary HPT
"Post-transplant patient still hypercalcemic despite functioning kidney" = Tertiary HPT
"High Ca, LOW PTH, history of lung mass" = PTHrP-secreting malignancy
"Brown tumor, subperiosteal bone resorption of radial side of middle phalanx (X-ray)" = Primary HPT (osteitis fibrosa cystica)
"Low urine calcium with hypercalcemia" = FHH (not adenoma - do NOT operate)
"Hypercalcemia + ACE elevated + bilateral hilar lymphadenopathy" = Sarcoidosis (granuloma-produced 1,25-OH-D)

I mean if I see a lot of notes, I will get triggered with that. I just want the question solving strategy, important concept I have to understand. Like I want like compact notes. I can't take too much of input because I have to remember all 19 subjects.

Got it. Ultra-compact, question-solving logic only. Here you go:

DI - SOLVE THE QUESTION IN 3 STEPS

Step 1 - What's the serum Na/osm? High → real DI. Low/normal → primary polydipsia (too much water drinking).

Step 2 - Give DDAVP. Does urine concentrate? YES → Central DI (brain not making ADH) NO → Nephrogenic DI (kidney ignoring ADH)

Step 3 - What's the context?

Head trauma / pituitary surgery / sarcoid / histiocytosis → Central
Male infant / lithium / hypercalcemia / hypokalemia → Nephrogenic
Pregnant → Gestational (vasopressinase destroys ADH, use DDAVP)
Psych patient, LOW serum Na → Primary polydipsia

Treat: Central → DDAVP Nephrogenic → Thiazide + low salt diet (NOT DDAVP) Lithium NDI → Amiloride

HYPERPARATHYROIDISM - ONE RULE

The key is: is Ca up or down, and is PTH autonomous or compensatory?

Primary = adenoma acting alone → ↑Ca, ↑PTH, ↓PO4 Secondary = CKD broke the kidney → ↓Ca, ↑PTH, ↑PO4 (compensation) Tertiary = CKD gland got so stimulated it went rogue → ↑Ca, ↑PTH after transplant

The one trap: Malignancy also causes ↑Ca but PTH is LOW (PTHrP doesn't show up on PTH assay). Lung/renal/ovarian cancer + high Ca + low PTH = PTHrP.

Treat: Primary/Tertiary → Surgery Secondary → Phosphate binders + Vit D + Cinacalcet

One image each to lock the concept:

Primary HPT on X-ray: subperiosteal bone resorption of middle phalanx + brown tumors DI on labs: high Na, low urine osm, high serum osm - that trio = DI until proven otherwise

what is ddavp

DDAVP = Desmopressin

Synthetic version of ADH (vasopressin).

Why it's better than natural ADH:

Longer acting
Resistant to vasopressinase (why it works in gestational DI)
Selective for V2 receptor (kidney water reabsorption) - no V1 effect (no vasoconstriction)

What it does: Binds V2 receptor on collecting duct → inserts AQP2 water channels → urine concentrates

Routes: Intranasal, oral, IV

Other uses beyond DI:

Hemophilia A (releases stored vWF and Factor VIII)
von Willebrand disease (type 1)
Nocturnal enuresis (bedwetting in kids)

Why it FAILS in nephrogenic DI: The V2 receptor is mutated or the kidney simply doesn't respond - no AQP2 insertion happens regardless of how much DDAVP you give.

like I have one question. Like in diabetes insipidus, there is either a problem in ADH production or the receptors are resistant or irresponsible to or unresponsive to ADH. So both of these could be the causes of nephrogenic sorry diabetes insipidus. So my question is, why in diabetic insipidus, the serum osmolality is high and why not normal? Because antidiuretic hormones main function or one and only function is to reabsorb water. So if it's not happening, then how come there is increase in serum osmolality? So you are telling that the water which has to come and join the blood is not coming. Hence there is high concentration, high concentrated blood osmolality. Hence serum osmolality is high.

Yes. You got it exactly right. Let me just confirm your logic cleanly:

Normal physiology: Blood gets concentrated → osmoreceptors sense it → hypothalamus releases ADH → kidney collecting duct reabsorbs water back into blood → blood gets diluted back to normal → osmolality stays ~285-295

In DI: ADH is absent OR kidney ignores it → collecting duct cannot reabsorb water → that water leaves in urine (large volume, dilute urine) → water is LOST from the body → blood has same solutes but LESS water → blood becomes concentrated = high serum osmolality

Your analogy is perfect:

"The water that was supposed to come back into the blood never came. So blood has fewer water molecules per solute. That's high osmolality."

Why urine is dilute at the same time: That unabsorbed water just flows out as urine. So urine = lots of water, very few solutes = low osmolality.

This is the key paradox NBME tests:

High serum osm + Low urine osm = DI (The blood is concentrated, the urine is watery - opposite of what should happen)

One more anchor: In SIADH it's the exact reverse - too much ADH, water stays in blood, blood gets diluted → low serum osm + high urine osm.

DI and SIADH are mirror images of each other. That's how you remember both.

MALIGNANCY DI LIKE PTHRP RULING OUT LABS I LINE

Malignancy (PTHrP) vs Primary HPT - Rule Out in 1 Line Each:

↑Ca, ↓PTH, ↑PTHrP, known cancer = Malignancy (PTHrP) ↑Ca, ↑PTH, ↓PO4, no cancer = Primary HPT (adenoma)

The one key: PTHrP is NOT detected by PTH assay → PTH comes back LOW despite high Ca. That low PTH with high Ca is your trigger to think malignancy.

Cancers that make PTHrP: Squamous cell lung, Renal cell, Breast, Ovarian, Bladder

Both cause: ↑Ca, ↓PO4, ↑urine Ca - because PTHrP mimics PTH action at the receptor

But PTHrP does NOT: stimulate 1-alpha hydroxylase (so 1,25-OH-D is NOT elevated, unlike sarcoidosis)

3-second rule for any hypercalcemia question:

Check PTH first →

PTH high = Primary or Tertiary HPT
PTH low + cancer history = PTHrP
PTH low + granuloma/lymph nodes = Sarcoidosis (↑1,25-OH-D)
PTH low + low urine Ca = FHH (don't operate)

Serum osmolality, urinary osmolality, and serum and urinary sodium.

4 Labs Across All DI Types + Differentials - Compact

Condition	Serum Osm	Serum Na	Urine Osm	Urine Na
Central DI	↑	↑	↓ (<300)	↓
Nephrogenic DI	↑	↑	↓ (<300)	↓
Primary Polydipsia	↓/normal	↓/normal	↓	↓
SIADH	↓	↓	↑ (>100)	↑ (>40)
Hypernatremia (dehydration)	↑	↑	↑	↓
Osmotic diuresis (DM)	↑	↑/normal	↑ (>300)	variable

The 2 lines that matter:

DI vs Primary Polydipsia: Both have dilute urine - but serum Na/osm is HIGH in DI, LOW/normal in polydipsia. Serum Na is your separator.
Central vs Nephrogenic DI: Labs are IDENTICAL. Only DDAVP response separates them - Central concentrates urine, Nephrogenic doesn't.
DI vs SIADH: Perfect opposites. High urine Na (>40) + concentrated urine + low serum Na = SIADH. Never confuse.

One anchor:

Urine Na >40 = kidney is dumping sodium = SIADH or adrenal insufficiency Urine Na <20 = kidney is holding sodium = volume depleted state or DI

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