Anatomy clinical correlates: Inguinal region

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Anatomy clinical correlates: Inguinal region

Metabolism HYMS year 3

Metabolism HYMS year 3

Anatomy of the abdominal viscera: Kidneys, ureters and suprarenal glands
Anatomy of the urinary organs of the pelvis
Anatomy of the female urogenital triangle
Anatomy of the perineum
Anatomy clinical correlates: Male pelvis and perineum
Anatomy clinical correlates: Female pelvis and perineum
Development of the renal system
Ureter, bladder and urethra histology
Kidney histology
Renal system anatomy and physiology
Hydration
Body fluid compartments
Movement of water between body compartments
Renal clearance
Glomerular filtration
TF/Px ratio and TF/Pinulin
Measuring renal plasma flow and renal blood flow
Regulation of renal blood flow
Tubular reabsorption and secretion
Tubular secretion of PAH
Tubular reabsorption of glucose
Urea recycling
Tubular reabsorption and secretion of weak acids and bases
Proximal convoluted tubule
Loop of Henle
Distal convoluted tubule
Renin-angiotensin-aldosterone system
Sodium homeostasis
Potassium homeostasis
Phosphate, calcium and magnesium homeostasis
Osmoregulation
Antidiuretic hormone
Kidney countercurrent multiplication
Free water clearance
Vitamin D
Erythropoietin
Physiologic pH and buffers
Buffering and Henderson-Hasselbalch equation
The role of the kidney in acid-base balance
Acid-base map and compensatory mechanisms
Respiratory acidosis
Metabolic acidosis
Plasma anion gap
Respiratory alkalosis
Metabolic alkalosis
Renal agenesis
Horseshoe kidney
Potter sequence
Hyperphosphatemia
Hypophosphatemia
Hypernatremia
Hyponatremia
Hypermagnesemia
Hypomagnesemia
Hyperkalemia
Hypokalemia
Hypercalcemia
Hypocalcemia
Renal tubular acidosis
Minimal change disease
Diabetic nephropathy
Focal segmental glomerulosclerosis (NORD)
Amyloidosis
Membranous nephropathy
Lupus nephritis
Poststreptococcal glomerulonephritis
Rapidly progressive glomerulonephritis
IgA nephropathy (NORD)
Alport syndrome
Kidney stones
Hydronephrosis
Acute pyelonephritis
Chronic pyelonephritis
Prerenal azotemia
Renal azotemia
Acute tubular necrosis
Postrenal azotemia
Renal papillary necrosis
Renal cortical necrosis
Chronic kidney disease
Polycystic kidney disease
Multicystic dysplastic kidney
Medullary cystic kidney disease
Medullary sponge kidney
Renal artery stenosis
Renal cell carcinoma
Angiomyolipoma
Nephroblastoma (Wilms tumor)
WAGR syndrome
Beckwith-Wiedemann syndrome
Posterior urethral valves
Hypospadias and epispadias
Vesicoureteral reflux
Bladder exstrophy
Urinary incontinence
Neurogenic bladder
Lower urinary tract infection
Transitional cell carcinoma
Non-urothelial bladder cancers
Congenital renal disorders: Pathology review
Renal tubular defects: Pathology review
Renal tubular acidosis: Pathology review
Acid-base disturbances: Pathology review
Electrolyte disturbances: Pathology review
Renal failure: Pathology review
Nephrotic syndromes: Pathology review
Nephritic syndromes: Pathology review
Urinary incontinence: Pathology review
Urinary tract infections: Pathology review
Kidney stones: Pathology review
Renal and urinary tract masses: Pathology review
Osmotic diuretics
Carbonic anhydrase inhibitors
Loop diuretics
Thiazide and thiazide-like diuretics
Potassium sparing diuretics
ACE inhibitors, ARBs and direct renin inhibitors
Endocrine system anatomy and physiology
Hunger and satiety
Insulin
Glucagon
Somatostatin
Diabetes mellitus
Diabetic retinopathy
Pancreatic neuroendocrine neoplasms
Parathyroid disorders and calcium imbalance: Pathology review
Diabetes insipidus and SIADH: Pathology review
Hyperthyroidism medications
Hypothyroidism medications
Insulins
Hypoglycemics: Insulin secretagogues
Miscellaneous hypoglycemics
Diabetes mellitus: Pathology review
Prostatitis
Prostate disorders and cancer: Pathology review
Prostate cancer
Prostate gland histology
Androgens and antiandrogens
PDE5 inhibitors
Adrenergic antagonists: Alpha blockers
Hyperthyroidism
Graves disease
Thyroid eye disease (NORD)
Toxic multinodular goiter
Thyroid storm
Euthyroid sick syndrome
Thyroid hormones
Hashimoto thyroiditis
Subacute granulomatous thyroiditis
Hypothyroidism
Thyroglossal duct cyst
Riedel thyroiditis
Thyroid cancer
Congenital adrenal hyperplasia
Primary adrenal insufficiency
Waterhouse-Friderichsen syndrome
Hyperaldosteronism
Adrenal cortical carcinoma
Cushing syndrome
Conn syndrome
Hyperparathyroidism
Hypoparathyroidism
Hyperpituitarism
Pituitary adenoma
Hyperprolactinemia
Prolactinoma
Gigantism
Acromegaly
Hypopituitarism
Pituitary apoplexy
Sheehan syndrome
Hypoprolactinemia
Constitutional growth delay
Diabetes insipidus
Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
Precocious puberty
Delayed puberty
Premature ovarian failure
Polycystic ovary syndrome
Androgen insensitivity syndrome
Kallmann syndrome
5-alpha-reductase deficiency
Autoimmune polyglandular syndrome type 1 (NORD)
Multiple endocrine neoplasia
Zollinger-Ellison syndrome
Carcinoid syndrome
Pheochromocytoma
Neuroblastoma
Opsoclonus myoclonus syndrome (NORD)
Adrenal insufficiency: Pathology review
Adrenal masses: Pathology review
Hyperthyroidism: Pathology review
Hypothyroidism: Pathology review
Thyroid nodules and thyroid cancer: Pathology review
Cushing syndrome and Cushing disease: Pathology review
Pituitary tumors: Pathology review
Hypopituitarism: Pathology review
Multiple endocrine neoplasia: Pathology review
Adrenal hormone synthesis inhibitors
Mineralocorticoids and mineralocorticoid antagonists
Synthesis of adrenocortical hormones
Cortisol
Testosterone
Estrogen and progesterone
Parathyroid hormone
Calcitonin
Adrenocorticotropic hormone
Growth hormone and somatostatin
Oxytocin and prolactin
Pituitary gland histology
Pancreas histology
Thyroid and parathyroid gland histology
Adrenal gland histology
Iron deficiency anemia
Alpha-thalassemia
Beta-thalassemia
Sideroblastic anemia
Glucose-6-phosphate dehydrogenase (G6PD) deficiency
Anemia of chronic disease
Lead poisoning
Hemolytic disease of the newborn
Autoimmune hemolytic anemia
Pyruvate kinase deficiency
Paroxysmal nocturnal hemoglobinuria
Hereditary spherocytosis
Sickle cell disease (NORD)
Fanconi anemia
Megaloblastic anemia
Folate (Vitamin B9) deficiency
Aplastic anemia
Vitamin B12 deficiency
Diamond-Blackfan anemia
Acute intermittent porphyria
Porphyria cutanea tarda
Hemophilia
Vitamin K deficiency
Hemolytic-uremic syndrome
Bernard-Soulier syndrome
Glanzmann's thrombasthenia
Immune thrombocytopenia
Thrombotic thrombocytopenic purpura
Von Willebrand disease
Disseminated intravascular coagulation
Heparin-induced thrombocytopenia
Factor V Leiden
Protein C deficiency
Protein S deficiency
Antiphospholipid syndrome
Antithrombin III deficiency
Hodgkin lymphoma
Non-Hodgkin lymphoma
Chronic leukemia
Acute leukemia
Myelodysplastic syndromes
Polycythemia vera (NORD)
Myelofibrosis (NORD)
Essential thrombocythemia (NORD)
Leukemoid reaction
Langerhans cell histiocytosis
Multiple myeloma
Monoclonal gammopathy of undetermined significance
Waldenstrom macroglobulinemia
Mastocytosis (NORD)
Microcytic anemia: Pathology review
Non-hemolytic normocytic anemia: Pathology review
Intrinsic hemolytic normocytic anemia: Pathology review
Extrinsic hemolytic normocytic anemia: Pathology review
Macrocytic anemia: Pathology review
Heme synthesis disorders: Pathology review
Coagulation disorders: Pathology review
Platelet disorders: Pathology review
Mixed platelet and coagulation disorders: Pathology review
Thrombosis syndromes (hypercoagulability): Pathology review
Lymphomas: Pathology review
Leukemias: Pathology review
Plasma cell disorders: Pathology review
Myeloproliferative disorders: Pathology review
Anticoagulants: Heparin
Anticoagulants: Warfarin
Anticoagulants: Direct factor inhibitors
Antiplatelet medications
Thrombolytics
Hematopoietic medications
Ribonucleotide reductase inhibitors
Topoisomerase inhibitors
Platinum containing medications
Anti-tumor antibiotics
Microtubule inhibitors
DNA alkylating medications
Monoclonal antibodies
Antimetabolites for cancer treatment
Anatomy of the thyroid and parathyroid glands
Pharyngeal arches, pouches, and clefts
Blood histology
Blood components
Blood groups and transfusions
Platelet plug formation (primary hemostasis)
Coagulation (secondary hemostasis)
Role of Vitamin K in coagulation
Clot retraction and fibrinolysis
Anatomy clinical correlates: Other abdominal organs
Anatomy of the male urogenital triangle
Membranoproliferative glomerulonephritis
von Hippel-Lindau disease
Klinefelter syndrome
Turner syndrome
Benign prostatic hyperplasia
Cryptorchidism
Varicocele
Orchitis
Testicular cancer
Epididymitis
Testicular torsion
Priapism
Penile cancer
Urethritis
Proteus mirabilis
Testicular tumors: Pathology review
Kidney stones: Clinical
Renal cysts and cancer: Clinical
Testicular and scrotal conditions: Pathology review
Anatomy clinical correlates: Inguinal region
Blood products and transfusion: Clinical
Venous thromboembolism: Clinical
Hypernatremia: Clinical
Hyponatremia: Clinical
Hyperkalemia: Clinical
Hypokalemia: Clinical
Metabolic and respiratory acidosis: Clinical
Metabolic and respiratory alkalosis: Clinical
Acute kidney injury: Clinical
Transplant rejection
Graft-versus-host disease
Cytomegalovirus infection after transplant (NORD)
Post-transplant lymphoproliferative disorders (NORD)
Rhabdomyolysis

Transcript

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The inguinal region, located near the groin, is found in the lower part of the anterior abdominal wall, and it contains several important structures that enter and leave the abdomen. Understanding the anatomy of the inguinal region is important for understanding common clinical conditions such as hernias, and many others!

Speaking of which, hernias occur when an organ or tissue protrudes through the wall of the muscle or tissue that normally contains it. The majority of hernias occur in the abdominal cavity or the inguinal region, through which subcutaneous fat, abdominal omental fat, or even abdominal viscera can protrude. In order for a hernia to happen, there is typically a weak point along the abdominal wall, such as a weak linea alba, previous surgical interventions that weaken the abdominal wall muscles, or pregnancy.

First, let’s look at anterior abdominal wall hernias. They can be divided into 4 categories: epigastric, umbilical or periumbilical, spigelian and incisional hernias. Epigastric hernias are caused by a weakened linea alba and are basically defects in the abdominal midline between the umbilicus and the xiphoid process. Then, there are umbilical or paraumbilical hernias, which are hernias through the umbilical ring or around the umbilicus. These are often found in children, because the umbilical ring is weak at birth, but can also be acquired in adults and frequently affect pregnant or obese individuals.

Spigelian hernias are found along the semilunar lines which are skin folds from the inferior costal margin of the 9th costal cartilage to the pubic tubercles and overly the tendinous insertions of the rectus abdominis muscle, as abdominal tissue can protrude through these areas of tendinous insertions. Finally, an incisional hernia can develop at the site of a prior surgical incision as the muscle and fascia is typically weakened, for example over the surgical site for an appendectomy.

Hernias can be classified as reducible, which means that they can be easily pushed back in the abdomen with position changes or manual pressure; or irreducible, which can’t be pushed back. Irreducible hernias can become either incarcerated or strangulated.

Incarcerated hernias are when the hernia contents are trapped and cannot be reduced, leading to swelling and edema of the herniated contents. With severe swelling, obstruction of blood flow to the herniated contents can occur, and this leads to ischemia and necrosis resulting in strangulation. Incarceration and strangulation can affect any protruding structure with a blood supply, such as the omentum and bowel.

Risk factors for developing a hernia include genetic defects, increased intra abdominal pressure, aging, obesity and pregnancy. Symptoms and signs of a hernia may include pain, discomfort, and a lump or a bulge in the affected area which may be exacerbated by increasing intra abdominal pressure such as coughing or laughing. Strangulated hernias can present with severe pain, nausea, vomiting, as well as tenderness and overlying erythematous skin changes.

Now, a similar concept to abdominal hernias is rectus abdominis diastasis, or divarication of the recti. This is when there’s a separation between the rectus muscles due to conditions that weaken and stretch the linea alba. This condition can also be congenital or acquired, and risk factors include obesity, pregnancy, connective tissue disorders or prior abdominal surgery. This particular type of hernia is not what we call a true hernia, because technically, the midline fascial layer of the abdominal wall is intact. This means that strangulation doesn’t occur.

Individuals affected by rectus abdominis diastasis present with a midline abdominal ridge that becomes more obvious when increasing the abdominal pressure and can disappear when the abdominal muscles are relaxed. Diagnosis is based on physical examination, and an abdominal ultrasound can be done to completely rule out a hernia.

Time for a quick quiz. What are the four main types of anterior abdominal wall hernias?

Now, let’s look at femoral and inguinal hernias. Femoral hernias occur when the hernia sac slips through the femoral ring into the femoral canal, below the inguinal ligament, medial to the femoral vein and lateral to the pubic tubercle and lacunar ligament. One important risk factor for femoral hernias is advanced age, as the femoral ring can widen with age.

Femoral hernias also tend to be more common in biologically female individuals compared to biological males; but don't get confused, as inguinal hernias are a more common type of hernia in both biological males and biological females. Now, as the space in the femoral canal is limited, femoral hernias can often become irreducible and incarcerated, and subsequently can cause bowel obstruction if there is bowel located in the hernia sac. In time, this type of hernia can become strangulated and cause bowel ischemia and necrosis.

On the other hand, there are two types of inguinal hernias; direct and indirect inguinal hernias, both occurring above the inguinal ligament when compared with femoral hernias.

Direct inguinal hernias occur when there is weakness of the transversalis fascia. In this case, the hernia sac pushes through the weak portion of the transversalis fascia, above the inguinal ligament. Here, it protrudes into an area called Hesselbach triangle, which is bounded laterally by the inferior epigastric vessels, medially by the lateral wall of the rectus abdominis, and inferiorly by the inguinal ligament. You should note, direct hernias do not pass through the deep inguinal ring and may only protrude through the superficial ring, therefore they have no direct route into the scrotum.

Indirect hernias occur when the hernia sac emerges lateral to the inferior epigastric arteries which is in contrast to direct inguinal hernias, and protrude through the deep inguinal ring into the inguinal canal, with the potential to extend distally into the scrotum. Indirect hernias are typically caused by a failure of the processus vaginalis to close in biologic males or the deep inguinal ring to close in biologic females. Remember that the processus vaginalis is an embryonic structure that precedes the descent of the testes through the inguinal canal. Normally, after the testes have descended to the scrotum, this structure closes up, but in some cases, it can remain open and allow for communication between the abdomen and the scrotum.

Inguinal hernias are the most common type of hernia in both biologically male and female individuals, and they occur much more frequently in males. Direct inguinal hernias are more common in older individuals, where indirect ones are more common in infants. Compared to femoral hernias, indirect inguinal hernias are less likely to become strangulated, with direct inguinal hernias the least likely to become strangulated.

Signs and symptoms of both femoral and inguinal hernias are a palpable bulge often exacerbated by increased intraabdominal pressure, pain, and discomfort. If an indirect hernia extends into the scrotum, then it can present as a larger palpable mass in the inguinal canal, and scrotal sac. If a hernia becomes incarcerated and strangulated, for example during a femoral hernia, this can lead to overlying erythematous skin changes, as well as nausea, vomiting, clinical obstruction, and extreme pain.

Okay, now let’s take a more practical approach on how to distinguish these different types of hernias based on clinical exam and anatomical landmarks. On clinical examination, femoral hernias are typically palpated lateral and inferior to the pubic tubercle. Both direct and indirect inguinal hernias occur above the inguinal ligament. Direct inguinal hernias push through the Hesselbalch triangle medial to the inferior epigastric artery, and may protrude into the superficial inguinal ring; so clinically, they can be palpated superficial or medial to the pubic tubercle.

Finally, indirect inguinal hernias protrude lateral to the inferior epigastric artery into the deep inguinal canal located at the midpoint of the inguinal ligament, and may extend through the inguinal canal and into the scrotum. Therefore, they may be clinically palpated with deep palpation using the tip of the finger, anywhere along the inguinal canal, medial to the pubic tubercle where they exit the superficial ring, or along the spermatic cord and into the scrotum. However keep in mind, you still may be unable to identify which type of hernia is occurring based on the clinical exam alone.

Okay, hernias can be resolved surgically with a procedure called herniorrhaphy - but sometimes complications arise. During hernia surgery, sometimes an artery called the aberrant, or accessory obturator artery, can be injured. Typically, the obturator artery branches from the internal iliac artery. However in up to 20% of people, there can be an additional branch coming from either the inferior epigastric artery or external iliac artery that either replaces the obturator artery or joins it, and this is called an aberrant or accessory obturator artery. This artery runs in close proximity to the femoral ring and courses along the superior pubic rami; so during hernia repair it can become injured or stapled.

Sources

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